Quiz Section: (Note, the material covered by the questions during each week may not correspond with the weeks in this course. These questions and answers were compiled by Jake Kulstad, a TA for this class in a previous quarter)
Difference between "Neuronal Doctrine" and "Reticular Doctrine"...
What is a "syncithium"?
-1870's or 19th century Golgi invented a neuronal "Silver"
stain.
-We DO NOT know why it only stains some neurons and not others.
-Ramon y Cajal used it to make great
illustrations of neurons.
-This new data (description of individual neurons) led to
the "Neuronal Doctrine". Before that the "Reticular
Doctrine " prevailed.
-A "syncithium" is just a big interconnected mass.
Parts of the neuron...
Cell body (soma), axon, dendrites, synaptic button,
axon terminal, myelin, nodes of Ranvier, axon hillock,
synaptic button, etc. Know all of these.
In a sensory neuron where is the axon hillock?
They don't have one... "the dendrites merge directly
into the axon".
The axon hillock is only necessary to converge signals
from the cell body.
Concentration gradients vs. Electrical gradients...
The Concentration gradient is ALWAYS present if
you are alive. It is not affected by the small flux of sodium
and potassium during an AP.
All cells in the body have potential energy...
This only refers to the gradients (electrical and
concentration) across the membrane. Only Neurons use this energy
Where do the values -70mV and +50mV actually come from?
These are just nice common numbers that we
use. They are physiologically relevant, meaning that most neurons have
responses in a similar range, but not all
use these exact numbers. Don't worry about it.
Events in the AP...
1.At threshold electrically gated Na+
channels open to begin the AP
2.K+ channels then open in response
3.Na+ channels close at the peak of
the AP
4.K+ channels close when resting potential
is reached
Know where these events
occur on the diagram of an AP.
Difference between "hyperpolarizations" and "depolarizations"...
Hyperpolarizations are negative, and depolarizations
are positive in this context (depolarizations push the
voltage closer to zero).
Are all AP's of the same intensity and duration?
In a given Neuron... yes.
Afferent and Efferent axons...
-Efferent neurons are Exiting a structure.
-Motor neurons are Efferent (exiting the nervous
system)
-Sensory neurons are classic, Afferent neurons.
-Some neurons could be considered to be both...
depending on your orientation in the brain ( a neuron can be
exiting one structure and coming into another...
so it depends on which you are talking about).
One, two, and three stage organisms...
One Stage - single neurons that provide basic reflexes
Two Stage - sensory and motor neurons
Three Stage - sensory, motor, and interneurons
Complex organisms (like us) are three stage systems.
Uni-polar, bi-polar, and multi-polar
**All neurons have only one Axon, but the
axon can split and make many different connections**
Unipolar - one process that acts as both dendrite
and axon
Bipolar - one axon and one dendrite
Multipolar - one axon and more than one dendrite
What are local interneurons, and what percent of the brain do they
occupy?
An interneuron is just not relaying info into
or out of a structure. "Most of the neurons of the [vertebrate] brain
are interneurons."
Macroglia
Oligodendricites - Myelinate CNS
Schwann cells - Myelinate PNS
Astrocytes - Scavenge debris and provide nutrition
Radial Glia - Guide developing neurons
How come glial cells are so much more common?
-How many Oligos or Schwann cells could each
neuron use if it is long?
-There are many Astrocytes providing support
as well.
-Remembering this can help to explain why
there are so many more glial cells.
Why do invertebrates not have myelinated axons?
-Just an issue of speed and distance.
-Vertebrate neurons that do not travel a long distance
or require a lot of speed are unmyelinated as well.
Why do AP's flow faster through thicker axons?
This is physics...please don't worry about
this right now... just remember that it happens.
How does the signal get from synapse to axon hillock, if it is not
an AP?
Graded potentials. These are relatively small and
decay over distance.
What is the role of the Na+ / K+ pump compared to gates/channels?
This is constantly working to maintain the
concentration gradient. The Na+/ K+ pump plays no direct role in
generating the AP itself.
What is the role of Chloride ions in generating the AP? How
about A-?
-These ions do not play a role in generating
the AP... that is why they are largely overlooked when we talk
about this subject.
-Cl- flows into the cell because it is attracted
by the + charge inside during the AP (the cell is permeable to Cl-
during the whole process).
-In a small way this slight inflow of negative
charge helps the neuron reach equilibrium, but it is negligible.
-Negatively charged Anions (A-) are just large,
charged particles (RNA, DNA, cellular processes, etc.) that do
not play any direct role in generating the
AP.
How do the gates know which ions to let pass?
Please don't worry about this.
What purpose do the synaptic vesicles serve in the synaptic terminal?
They hold small amounts of neurotransmitter and
keeps them ready for release (exocytosis). The vesicles also protect
them from degradation, etc.
Can you explain/define spatial and temporal summation?
Temporal summation (root is Latin for "time") would
be EPSP's or IPSP's from a single source that occur in rapid succession.
If they are close enough together in time they will build upon each other
and "sum up" to a greater excitatory or inhibitory force than each would
alone. Spatial summation involves input (EPSP's or IPSP's) from different
sources that arrive in the Axon Hillock at the same time and can add up
or inhibit each other (an equal IPSP and EPSP could reach the axon hillock
together and equate to "zero" excitation or inhibition).
What is the difference between autoreceptors and heteroreceptors?
Remember the roots of the terms... "auto"
meaning self, and "hetero" meaning other.
-An autoreceptor is feedback in the form of neurotransmitter binding
to specific receptors on the axon terminal that released it.
-Heteroreceptors take in excitatory or inhibitory input from other
neurons. This info can make it more or less likely that neurotransmitter
will be released even after an action potential has already "decided" to
occur.
What is the importance of Otto Loewi's experiment with the frog hearts?
Loewi proved that synaptic transmission occurs
through chemical messengers instead of electrical signals. The Vagus
nerve stimulated the release of acetylcholine which slowed the heart by
way of muscarinic receptors.
How did Sherrington decide that there must be some sort of communication
across synaptic gaps instead of the continuation of an action potential
through his work with reflexes?
-He noted a delay in the reflex that would
not occur if the signal simply went at the speed of an action potential.
-He showed temporal and spatial summation.
-He showed excitation and inhibition through
the same pathway.
We know that the brain and the spinal cord work together, but is
the spinal cord an actual "separate" unit, or is it totally dependent upon
the brain for its functioning?
Sherrington's work began to answer this question
when he severed the spinal cord of his subjects in order to perform his
experiments. In terms of providing quick and automatic reflexes the
spinal column can operate independently. The reflex happens before
the brain is even "told" that it will be carried out.
Could you explain the divisions of the PNS and their functions?
The primary divisions of the PNS are the Somatic
and Autonomic nervous systems. The somatic system provides
the classical afferent (sensory) input, and efferent (motor) output.
The autonomic nervous system is divided into the Sympathetic "Fight or
Flight", and the Parasympathetic (rest, digest, and conserve energy) responses.
How are EPSP's and IPSP's similar and dissimilar to action potentials?
**The following is from Dr. Olavarria's class notes...
1. Characteristics of postsynaptic potentials:
-Variable size:
They can be of different
size (graded, not all-or-nothing). The size of Postsynaptic potentials
depends on the amount of transmitter available in the cleft, and on the
number of postsynaptic channels that open.
-Variable duration:
Postsynaptic ions channels will remain open as long
as transmitter interacts with the receptor.
2. Differences between Action Potentials and Postsynaptic Potentials:
Action Potential Post-Synaptic Potential
All-or-none, regenerative Graded potential, variable in size and duration
Has threshold No threshold
Voltage gated channels Chemically-gated channels
Specific ion channels Non-specific ion channels
Always depolarizing Can be depolarizing or hyperpolarizing
Why are EPSPs smaller in voltage than action potentials?
If Na+ channels and K+ channels are both opened
up the net effect would be a maximum increase in resting potential to 0mV.
One of the main reasons that APs are so large is due to the fact that the
Na+ channels open themselves up once threshold is reached (the depolarization
spreads like a fire). The excitation provided by EPSPs comes in the
form of a limited number of the Na+ channels opening in response to a neurotransmitter
(Glutamate, for example) and provides a smaller, local effect that degrades
as it travels to the axon hillock.
What is hydrolysis, exactly?
A good way to think about this process is
that it breaks up neurotransmitters to make them inactive. A good
example is acetylcholine... AchE (acetylcholinesterase) hydrolyzes
Ach by breaking it up into "choline" and an "acetyl" group which are inactive
when separated. The choline is taken back into the cell to be reused
in this case.
How do agonistic and antagonistic drugs affect Synaptic transmission?
Agonists enhance, and antagonists inhibit
neurotransmission. For more detail you need to look at each individual
case.
How does physostigmine or neostigmine treat Atropine poisoning?
Atropine is an acetylcholine (Ach) antagonist.
By using these two Ach esterase inhibitors you can reduce the hydrolysis
of Ach and make sure more is available to counteract this poisoning.
What is the difference between neurotransmitters and neuromodulators?
Neuromodulators simply enhance or inhibit
the effects of neurotransmitters and do not convey excitatory or inhibitory
information on their own.
Are transmitters the only way that postsynaptic channels can be opened?
Neurotransmitters are responsible for "ionotropic"
and "metabotropic" opening. Channels can also be opened "mechanically",
but we did not dwell on that in class.
What is the synaptic cleft?
This is just another term for the space between
the axon terminal and the post-synaptic neuron...what we generally call
the synapse.
If an axon branches does the action potential travel down all branches
with the same effect?
Yes... the AP will continue down all branches, and most neurons
release the same neurotransmitter or combinations of neurotransmitters
at all axon terminals.
Please clarify electrical synapses. Why isn't memory or learning
possible in this context?
An electrical synapse allows the action potential
from one neuron to pass directly on to another through special channels.
If the firing of one neuron ALWAYS led to the firing of a second neuron
there could be no modulation of the effect. Meaning... for memory
or learning to occur the neurons must be able to alter connections and
responses to input. It also allows for much more diverse behavior
if input from multiple sources is taken into account.
What is the effect of "re-uptake inhibitors" like Cocaine?
By blocking the re-uptake of a neurotransmitter
you can effectively keep more of it present in the synaptic cleft. For
cocaine it leads to an abundance of dopamine which should make you feel
fairly good. Your neurons respond by shutting down production of
dopamine... so when the drug wears off there is less of it available and
the "hang over" occurs.
How specific are receptors... can they respond to different molecules?
Receptors are fairly selective... remember
the lock and key. Some drugs can attach to receptors even if the
do not match exactly. These may have an altered (reduced) effect,
or may have no effect at all. In come cases a drug may simply block
the receptor so that none of the intended neurotransmitters can reach it.
It all depends on the receptor and the molecule that you are talking about.
What is CSF, and how does it circulate in and out of the brain?
Cerebral Spinal Fluid is basically very pure, filtered,
salty water. It maintains its overall fluid mass by a constant infusion
of highly filtered blood plasma through the choroid plexus in all of the
ventricles. After introduction into the ventricles it flows through
the central canal and out into the sub-arachnoid space. It eventually
is recycled as it re-enters the blood supply through specialized channels
in the sinuses.
What are the 3 functions of CSF?
The CSF provides cushioning and protection for the brain.
It serves as a nutritive storage medium. It is also a valuable diagnostic
tool to determine what pathogens or general conditions exist in the brain
with a relatively non-invasive spinal tap.
What are the major sections that the brain can be cut into? (Coronal,
Sagittal, Parasagittal, and Horizontal)
When you cut the brain into a Coronal section remember
that you can see all of the gyri and sulci very prominently and it looks
like a crown... hence the term "coronal". Sagittal cuts are made
down the midline of the brain dividing it into the right and left hemispheres.
Parasagittal sections are made parallel to a sagittal cut, but not exactly
down the midline. Horizontal cuts are simply made perpendicular to
the orientation of the "vertical" coronal sections.
Can you review the concepts of dorsal, caudal, ventral, anterior,
and posterior and the differences between the head and the body?
You need to have diagrams for this... If you point your head
upwards to look at the ceiling (pretend you are anatomically oriented like
a salamander) all of the reference points are the same for the head and
the body. Rotate all reference points for the head accordingly if
you are facing forward. Dorsal is the top (think of the dorsal fin
on a dolphin), ventral is the bottom (stomach), anterior is front, posterior
is behind, caudal is the same as posterior (think tail since caudal means
of or referring to the tail), and rostral is the same as anterior (rostral
= nostril).
What is the function of the cerebral ventricles?
They house the choroid plexus for CSF production.
They also function as a CSF reservoir helping to ensure that the brain
is adequately surrounded. If there is neuronal loss due to a neurodegenerative
disorder or some form of trauma, the size of the ventricles will effectively
grow to compensate for the reduction in the number of living neurons, or
overall neuronal density.
Please explain the terms "orthodromic" and "antidromic".
These terms were used when outlining methods for determining
that certain axons within the spinal cord were connected to distant neurons
in the somatosensory and motor cortices. By using an electrode researchers
were able to stimulate an axon terminal and record the result of an action
potential that traveled backward up to the soma. This was an antidromic
impulse (simply an AP travelling in reverse which would never happen without
the input of an experimenter). The opposite is orthodromic (travelling
the direction that an AP usually leads), simply an experimentally produced
action potential to see where the axon leads with recording equipment.
How can you tell whether transport is retrograde or anterograde?
Do not confuse this with orthodromic and antidromic!
Anterograde and retrograde transport is always happening up and down an
axon. Retrograde is backwards in relation to an action potential
(from axon terminal to soma). Anterograde is from soma to axon terminal.
Researchers simply take advantage of this natural transport mechanism to
introduce dyes which trace the pathway of the axon to show us which connections
it makes.
What is the role of anatomical tracers in determining neuroanatomy?
By using anterograde and retrograde transport we can determine
the connections that individual neurons or populations of neurons make
in the brain and throughout the nervous system.
Can you tell me the functions of the ectoderm (outside), mesoderm
(middle) and the endoderm (inside) of an embryo?
These terms are in reference to the entire developing
embryo in its earliest stages. The ectoderm forms the skin and brain.
The mesoderm gives rise to the muscles, and the endoderm ends up forming
the gut.
Do the number of wrinkles in the brain relate to intelligence or
some sort of behavior or characteristic?
The answer is no. Psychologists many years ago hypothesized
this and tested it extensively without finding any significant or distinguishing
features related to intelligence or specific skills. Einstein's brain
was also studied to a great extent, and they may have found that he had
a few more fully formed gyri in his Medial Temporal Lobes, but you need
to read this on your own. I would call this line of investigation
"pseudo-science" if you will forgive the personal commentary.
What is the difference between the neural plate and the neural tube?
The neural plate is the original sheet of cells that begins
to form the brain. This sheet folds over onto itself to produce the
neural tube as development progresses. This is the basis for the
formation of the ventricles.
Could you explain migration, proliferation, aggregation, and
"inside out" development?
Inside out development was a reference to the order in
which the layers of the cortex form during development. Neurons proliferate
and migrate outward to layer VI (the innermost) first, and then other neurons
migrate outward from the neural tube to form subsequent layers. The
term migration is used much as it is for the movement of ducks with the
change of seasons. Entire populations of neurons are produced (proliferate)
around the neural tube (germinal layer) and they move (migrate) outward
along the path set up by the radial glia to find their new homes for life.
Once they find their target they tend to form groups of neurons (aggregation)
which we called nuclei before.
Since blood goes to the brain and creates CSF, is this how oxygenation
of the brain happen? And how does this relate to the blood/brain barrier?
The answer is "no". The CSF is completely
separate from the Blood Brain Barrier (BBB). The BBB is in place
around every blood vessel which flows through the brain. Glucose,
oxygen, carbon dioxide, and everything else passes through the BBB all
throughout the brain and reaches neurons through astrocytes which aid in
this process.
We have learned that the brain has a lot of wrinkles (gyri and sulci).
Which tissue matter makes up these wrinkles?
Both grey matter and white matter are present in each
gyrus. The grey matter (or cell bodies) is on the outside, while
the white matter (myelenated axons) is on the inside connecting these somas
with other neurons in the brain.
What were the weights for the brain at different developmental stages?
At birth the brain is approximately 300 grams, at 12 months
it is about 1,000 grams, whereas a full-sized adult brain is approximately
1,200 grams.
What is the difference between dura matter and pia matter?
Dura Matter is Latin for "Tough Mother", Pia Matter
is Latin for "Pius Mother". This should help to differentiate.
What is the purpose of the sinus and is it what gets congested during
a cold?
The sinus that we are referring to is different
from our nasal sinuses... please do not confuse them. Sinus is a
general term for a cavity and is used in both cases.
In class it was mentioned that damage to the sinus can cause extreme
bleeding and possibly even death. How is this possible?
It could be breached by physical trauma, but possible
more significantly it can be injured by internal pressure. The sinus
is a major blood vessel , but it differs in that it cannot expand due to
the dura matter surrounding it. Unlike most blood vessels it is inflexible,
and as such is not easily repaired.
How does Parkinson's disease affect the substantia nigra?
The exact mechanisms by which this disease leads to neuronal
damage are largely unknown. For some reasons the neurons in the Substantia
nigra, basal ganglia, and amygdala are particularly susceptible to this
disease. Parkinson's generally leads to a reduction in the critical dopaminergic
neurons in the substantia nigra which are essential for motor control among
other things.
What is the functions of the Thalamus?
Thalamus serves primarily in processing sensory input
and channeling it to the proper areas in the cerebral cortex.
What do the Superior and Inferior Colliculi do?
The superior colliculus serves primarily to coordinate
basic visual reflexes and eye movement. The inferior colliculus is
important in producing basic auditory reflexes and relaying of information.
It is of particular interest to note that in fish (for example) their brain
is dominated by these two structures. This would point out the very
important role of the colliculi in their primarily reflexive feeding patterns
and existence.
Please explain the timing of "apoptosis," that is massive, programmed
cell death... Is this related to the cell death that occurs later in childhood
(as a "pruning" process)?
Apoptosis is a term for programmed cell death at any stage.
During development many neurons undergo apoptosis (die) if they do not
make correct connections. The "pruning" process that occurs later
during childhood is the same type of cell death , only for a different
reason. Why this happens... I don't remember offhand. Scientists
have pointed out that the acquisition of foreign languages is vastly easier
before this takes place. This would seem to be associated.
Where does the term "hydrocephalus" come from?
From the root hydro (water) and cephalus (of or relating
to the brain). It is the term for the build-up of pressure from excess
fluid (CSF) in the brain. This can lead to neuronal damage.
Several questions about neuron production-development... Prof.
Olavarria mentioned the difference in amount of neurons "kept alive" between
Schwarzenneger and himself. If a person makes physical changes in
life do new cells grow (should he/she make more muscle) or die (if he/she
loses muscle or a limb)? How late in life do cells continue
to be produced and migrate?
After neuronal proliferation has ceased no new neurons
are produced in the brain. The only thing that neurons can do in
response to environmental changes is to alter their connections with others.
This provides the basis for learning and adaptation over the years without
the introduction of new neurons.
What are the factors that affect Axon Growth and Synapse Formation
(blueprint hypothesis, chemoaffinity, Hebb's postulate, and fine-tuning
of connections by spontaneous and experience-evoked activity)?
The first hypothesis concerning the directing of neuronal
connections was the "blueprint Hypothesis". This stated that develping
neurons
followed a set path to guide them to their destination. This
does happen, but Sperry proved that sensory neurons that are misplaced
can still
find their way to the correct place in spite of incorrect physical
orientation. This led to the advancement of the chemoaffinity, or
chemical
hypotheses. In this paradigm there are chemical gradients that
help developing axons find their exact target.
Once in the correct place synaptic connections are
strengthened or "fine-tuned" by activity. Spontaneous activity is
naturally occurring
patterns (remember the example of the AV node in the heart) that do
not need external stimuli. Evoked activity refers to the strengthening
that
occurs due to stimulation of sensory neurons from external stimuli
(i.e. the continued development of visual topography after the eyes have
opened). Hebb stated that "Neurons that fire together, wire together".
This supports the fine tuning aspect in that neurons that fire with the
same pattern or frequency will have their connections strengthened,
and thus "wire together".
These three all work in conjunction with each other
and provide redundancy. Some axons are able to find their way to
the correct spot
without a blueprint, but some others cannot. Remember the Probst
bundles that formed when the Corpus Callosum was cut? These callosal
fibers could not find their way and formed bundles of axons that were
misguided.
What was sperry's experiment with the frog eyes, and how is that
related to neuron/axon migration? How did the frog see things
upside down?
When Sperry cut the optic nerve and rotated the eye 180 degrees
the axons still found their way to the exact spot that they should have
if
they had been oriented properly. This meant that their actual
position had no effect on their guidance. Since the receptors that
were involved
in the transduction of stimuli were upside down the entire visual representation
of the "frogs world" was upsidedown.
What is the role of guideposts.
Guideposts are neurons which direct developing axons
as they grow. They are like signposts guiding axons and are important
for providing
a "blueprint" for axons to follow.
What are growth cones and filopodia?
The growth cone is the area of a developing neuron
that guides it through its environment. The filopodia are the little
extensions that reach
out from the growth cone to "touch", "smell", and "guide".
What is the role of cell adhesion molecules?
When the axon finally finds its target the cell
adhesion molecules help it to stay anchored and receive the neurotrophic
factors which are
essential for its survival.
How does the axon and target "sing the same tune"?
The "singing" that we are concerned with here is
in reference to neurons that are firing with the same patterns of activity.
This is the basis for
Hebb's Postulate.
What is the tetnus (or tetanic stimulation), its function, and relation
with LTP?
The tetanus is the technical name for the 100Hz
pattern of action potentials that creates LTP.
What are the properties of LTP (cooperativity and associativity)?
Cooperativity in this context refers to the ability
of different neurons to produce a tetanus together. If one is firing
at a high rate (but below
the 100 Hz rate of tetanic stimulation) a second neuron could fire
at the same time to produce a rate that reaches the necessay level for
LTP to
occur. This is much like the Spatial summation of post synaptic
potentials.
Associativity is the pairing of weak stimulus
with a strong one (much like Pavlovian conditioning). When a strong
synapse produces a
tetanus, another synapse can take advantage of this state if it fires
at the same time. Since the post synaptic neuron has been depolarized
and
mg++ is no longer blocking the NMDA receptor the weak stimulus can
trigger the influx of ca++ and strengthen its association through LTP
just like a synapse that was strong enough to produce a tetanus on
its own.
What is LTD?
LTD stands for Long Term Depression. This
is the opposite of LTP.
Does it matter or affect LTP when Nitric Oxide synthesis is blocked?
Yes... LTP itself has been shown to be eliminated
if NO synthesis is blocked. Retrograde transmitters are important
for providing signals to
the presynaptic neuron, but the exact role is unclear so we do not
focus on NO with any more detail than that in this class.
Will you explain the water experiment again?
The Morris Water Maze is a very common learning
paradigm used to test the spatial abilities of rats. When rats are
place in this small,
circular pool they are very motivated to find a platform that is hidden
from sight just below that waterline of the pool. With training they
learn
to quickly find the position of this platform. Rats that have
undergone experimental treatments that affect learning and memory (or LTP
in this
instance) show a reduced ability to learn this spatial task, and spend
more time than controls searching for the platform even after repeated
trials. There are many experimental tasks that can be performed,
but this one is fairly effective and well validated.
If you block NMDA receptors will it interfer with learning?
If NMDA receptors are blocked, then LTP cannot occur.
The in-class example indicated that rats which cannot produce LTP were
unable
to learn the position of the escape platform in the Morris Water Maze
test.
What is the difference between transduction and coding?
Transduction is the transformation of physical energy
(sensory input) into graded potentials or action potentials by a sensory
neuron. Coding is the pattern of activity that "represents" the external
stimulus.
There are transduction receptors and coding/transduction receptors,
are there coding only receptors?
No... all receptors transduce, and some do both.
What is a neurotrophic factor?
This a generic term for a substance which is critical
for neuronal maintainenance or provides essential nutritive factors to
a neuron. The ones
which we referred to are BDNF (brain derived neurotrophic factor) and
NGF (nerve growth factor).
What does "in vivo" mean?
It is a reference to something done inside a living organism.
in vitro is the opposite... an experiment done in an artificial environment.
What is fasciculation?
The adjective form of the term is to be arranged or formed
into a bundle. In this context the developing neurons migrate along radial
glia that would most likely look much like bundles of neurons following the
same path (or blueprint).
Drugs and Addiction
(Guest Lecturer: Dr. T. Jones)
Of the behavioral classes of drugs which ones are agonists and which are
antagonists? Sedative Hypnotics, Stimulants and convulsants, Opiates, Psychedelics,
Antipsychotics, and Neurologic drugs.
Please be careful here... many drugs act in different ways
even within these classes. The terms agonist and antagonist have nothing
to do with the final behavioral outcome of drug administration. Note:
An agonist that mimics an inhibitory neurotransmitter can have similiar behavioral
effects as an antagonist that decreases the efficacy of a related excitatory
neurotransmitter... think about it.
Dr. Jones talked about the break down of ethyl acohol to acetaldehyde and
finally to acetic acid when she was talking about having hang overs but she
never really said how this breakdown process (acetaldehyde dehydrogenase) causes
the hang over sensation and symptoms. Could you explain this?
The real specifics are too much for us (yes, you and me).
A large part of the hangover is the presence of acetylaldehyde in our bodies.
This substance is toxic and makes us feel sick when it is present. After
it is finally converted to acetic acid and eliminated (through urine) we can
begin getting on with our daily lives.
What exactly do the presynaptic autoreceptors do to neurotransmitters, or
what can they do? (in relation to Dr. Jones' talk)
The autoreceptors are simply a feedback mechanism to let
the axon terminal (bouton) know that there is neurotransmitter present in the
synaptic cleft. This indication leads to a decrease in neurotransmitter
production and release.
What exactly is addiction? Is just a craving for the substance?
What is withdrawal? Is that just imbalance of the natural homeostasis
due to administration of a drug?
Addiction and physical dependence are two different things.
Addiction implys negative societal implications in the face of repeated efforts
to stop administration of a substance. Physical dependance is the presence
of withdrawal symptoms. Yes, withdrawal is the net effect of the body's
response to a drug (opposite of the drug's effect) after the drug has worn off.
The body tends to have a slower and more prolonged response.
Do all the pathways and axons that disappear after the monkey took ecstasy
ever fully come back?
Based on the literature that I am aware of there is never
complete recovery to original levels for serotonin in the frontal cortex.
I'm confused about the long-term effects of alcohol. Why are the long-term
effects on NMDA and GABA receptors opposite to the immediate-term effects?
When Dr. Jones was talking about the "long term effects"
of alcohol use she was referring to the body's reaction to chronic use.
Since alcohol is a sedative the body moves toward homeostasis by producing the
opposite reactions. The body's increase in the efficacy of NMDA
receptors and decreased efficacy of GABA receptors with chronic use/abuse is
the opposite of alcohol's mechanisms of action. This is an example of
functional tolerance.
Why does withdrawl from heavy long-term alcohol use cause neuronal excitotoxicity?
Excitotoxcicity can result from a very abrupt withdrawal
after long-term alcohol abuse. The body responds to this repeated administration
of a sedative with overall neuronal excitability. Without alcohol present
they can get so excited that they actually become apoptotic and kill themselves.
Please explain how CNS depressants can have neuronal effects that both increase
the function of voltage-gated Ca2+ channels and reduce flow of Ca2+ into voltage
gated channels.
One immediate effect of a sedative is to reduce the flow
of Ca++ into the cell (thus reducing APs) . The long-term cellular adaptation
to chronic use is the opposite as the cell strives to maintain homeostasis in
the face of abuse.
Could you explain metabolic tolerance, functional tolerance and conditioned
tolerance.
A classical example of metabolic tolerance is an increase
in the enzyme acetaldehyde dehydrogenase for breaking down ethyl alcohol.
One avenue of functional tolerance is a "downregulation" of receptors for the
drug at the synaptic level. Conditioned tolerance is the "state dependant"
adaptation that Dr. Jones mentioned. When a user enters an environment
that is closely associated with the administration of a drug the body initiates
a response to it before the drug is even taken. All three of these are
mechanisms by which the body strives to maintain homeostasis in the presence
of, or in anticipation of a drug.
Why does increased breakdown of a drug increase tolerance?
With an increased ability to break down (metabolize) a substance
you need to take more of it to produce the desired effect.
What does dLGN stand for?
This is the "dorsal Lateral Geniculate Nucleus".
What does rhodopsin do, exactly?
Rhodopsin is the photopigment that we are focussing
on. When a photon of light hits rhodopsin it hydolyzes it and splits
it into its constituents (Retinal and Opsin). This starts the "cascade"
reaction that amplifies this signal, takes some time to occur, and eventually
leads to the hydrolysis of cyclicGMP. This reduces the concentration
of cGMP and hyperpolarizes the membrane, thus ending the flow of "dark
current".
Can you go over the "dark current" phenomenon?
When there is no light hydrolyzing rhodopsin
the cyclicGMP is in high concentration and it keeps the Na+ channels open.
This causes a slight depolarization that contributes to an increase in
the graded potentials produced by receptors. This is only present
without light... light actually hyperpolarizes the membrane (back to -70mV)
when it strikes a receptor.
How does the action potential or electical response work in visual
receptors?
I'm just confused with the backwards polarity thing regarding depolarizing
and hyperpolarizing.
Retinal receptors (rods and cones), bipolar
cells, horizontal cells, and amacrine cells do not produce action potentials.
They simply produce graded potentials that determine if the ganglion cells
will actually fire (this is the first AP). Dr. Olavarria did not
focus on the inhibitory effect of receptors in class, but I will mention
it for the sake of clarity even though it won't be on the test... Dr. Olavarria
did
mention
that the one important caveat here in that it is important for a change
to
occur for information to be passed. When light strikes the receptors
the result is actually a decrease in their membrane potential (back down
to -70). This increases the chances of a retinal ganglion cell firing
since the receptors have an inhibitory effect on them. This
is "double negative" or "disinhibition". If this is confusing ask
me in person, or don't worry about it since this was not focussed on in
class.
Could you go over the phototopic system, especially where he talks
about the little convergence from rods to ganglion cells.
We talk about convergence in the sense that several
rods will synapse with a single bipolar cell and connect to only one retinal
ganglion cell. The signals converge, or funnel into one channel and
combine their intensities (effectively amplifying the signal at the loss
of acuity).
What are invaginations?
These are simply a fancy name for the indents in
cones. Rhodopsin is found in the membrane of these invaginations.
How is it possible that light is not refracted or reflected as it
passes through all of the cells of the retina before it gets to the
rods and cones?
Your text states that light is distorted very minimally
as it passes through these layers. Presumably, we are unable to detect
this level of distortion.
What part of the eye does color blindness effect?
Your text mentions that you can get color blindness
if one or more populations of cones in our retina do not work properly.
This is commonly genetic.
Can rods and cones get damaged and is that what causes blindness?
You certainly could get blindness due to physical
damage or developmental irregularities in the rods and cones. Blindness
can also occur when essential areas of the occipital cortex are damaged
due to stroke, injury, etc.
Did the proff. say that the photopic is more red based and the scotopic
is more blue? (If so, why? If rods are mainly for black and white vision)?
This is in reference to the "Purkinje Effect".
This has to due with the physical responses of the two systems and actually
has nothing to due with the coding of color. Rods respond greater
to light of shorter wavelengths even though they actually do not code it
as a particular color, only intensity.
Why are cone fed circuits low convergence and rod fed circuits high
convergence?
Cones connect with Retinal Ganglion cells
at a ration of 1 to 1. There is actually NO convergence (amplification
due to "funneling") of information in this connection. Rods attain
their sensitivity by having many receptors connect with a single ganglion
cell. The rods sharing a single ganglion "converge" to sum up these
small transductions into a signal that can be sent on to the brain.
Why do we have more rods than cones when our world is in color?
Shouldn't we have just as many cones?
Due to the "convergence" of signal in the
rod system there are several receptors connected with each ganglion cell.
This helps to explain why we have so many with respect to cones.
We must assume that we have as many cones as are necessary to provide a
very detailed map from the fovea, and that more cones were not deemed necessary
by evolutionary processes.
What occurs during the "cascade" of chemical reactions after rhodopsin
is activated by light?
We were not given many specifics during lecture
in class. Just remember that the cascade takes a little bit of time,
effectively amplifies the signal (geometric progression), and ends up hydrolyzing
cyclicGMP. This leads to the closing of the Na+ channels in the receptors.
During the beginning of class the professor mentioned that the optic
nerve is from the region of Diencephalon...but I'm not sure if that's what
he really said.
We were shown this to answer questions that
students had about a particular part of the last exam. During development
the future retina emerges from the diencephalon.
What is the fuction of photopigment?
Rhodopsin is the photopigment that we are talking
about. It is essential for the transduction of photons of light into
an electrical stimulus that our brain can decipher.
What is 11-cis-retinal?
This is the terminology that your book uses...
Dr. Olavarria called it "Retinal". Retinal and Opsin are two
proteins that combine to form Rhodopsin.
What are photons?
A photon is an individual particle of light.
Light is confusing in this respect since it behaves in ways that make it
look like single particles (photons), and it also travels as a wave.
Don't worry about this, your friends in the physics department dream about
this stuff all the time.
I understand the concept of how the scotopic system has poor acuity,
but I'm not clear on how the photoscopic system has poor sensivity.
Sensitivity is achieved in the scotopic system since
so many rods converge to amplify a weak signal. In the photopic system
the connections are 1 to 1 (low convergence) so this system cannot amplify
a weak signal and is less sensitive that the scotopic system.
The tapetum... what was the equivalent in humans and why is this
important?
The tapetum is equivalent to the choroid layer in
humans. Our choroid is black to make sure that there is no excess
light bouncing around to decrease visual acuity. For relatively nocturnal
animals like deer and raccoons the tapetum reflects light to help gather
as much of it as possible in low light conditions.
What was professor charting when he showed the degress of field of
vision in rods vs. cones?
The main purpose of this is to show that there is
a high density of cones in the fovea, and that the highest concentration
of rods occurs approx 20 degrees off-center. In order to see stars
that are very weak you should look slightly to the side to make sure that
the light is striking the point of highest density for your rods.
The chart also showed the location of your blind spot nicely.
What are the functions of the 5 layers of receptor cells, horizontal
cells, bipolar cells, amacrine cells, and ganglion cells in the retina?
We have been focussing on the importance
of the receptors (rods and cones) a lot. These primarily synapse
on bi-polar cells which mainly connect to the retinal ganglion cells.
It is in the ganglion cells that the first AP occurs and sends a signal
to the dLGN. We have not been focussing on the role of horizontal
and amacrine cells in this system. Just know that they are there,
where they are located, and that they contribute to the "pre-processing"
of visual stimuli even before they are sent to the dLGN.
What are the three muscles that control movement in the eye called?
Don't worry about this... it wasn't mentioned in
lecture.
Visual System, Auditory System
Regarding the organization of the visual pathway,
how is it that half of the left eye goes to the left side of the brain?
The retinal ganglion cells send their axons to the
dLGN forming the optic nerve. The two optic nerves converge at the
optic chiasm and at this point axons from ganglion cells representing the
nasal portions of the retina cross over to the contralateral side of the
brain. This makes sense since the left side of both eyes goes to
the left side of the brain and vice versa. How this actually happens
from an evolutionary perspective is beyond my comprehension.
Do the ipsilaterial and contralateral projections
describe how messages get to the same or opposite side of the brain?
Yes, ipsilateral means
"same side" and contralateral means "opposite side" with respect to any
part of the brain.
Please clarify the term retinoptically organized and what is a retinotopic
map?
These terms are used to portray the notion that
each retinal ganglion cell is responsible for a particular portion of the
visual field. These are "mapped out" in the cortex in an organized
fashion and correspond to the visual field itself.
Please clarify the magnocellular and parvocellular pathways.
Also, the Ventral Stream is the "What" part of the visual system and the
Dorsal Stream is the "Where" of the visual system. How do these systems
work together?
Magnocellular (large cells) and Parvocellular (small
cells) pathways create the ventral and dorsal streams of our visual perceptions.
The parvocellular cells are found mostly around the fovea (cone driven)
and are best for conveying details (the "what" information) which are processed
in temporal areas from the ventral stream of information. The magnocellular
cells have larger receptive fields and are distributed throughout the retina.
These respond well to movement, and convey "where" information along the
dorsal stream. They work independently to process these two types
of information, which is why lesions to these separate areas of cortex
lead to problems in different aspects of visual processing. Dr. Olavarria
mentioned that the information from these two, separate streams is later
integrated in the prefrontal cortex in order to create a "coherent" and
integrated "view" of our world.
Could you please explain the difference between simple and complex
cells?
This was not mentioned in lecture, so don't worry
about it.
Is there a difference between the bipolar cells for cones and rods?
For our purposes we won't worry about this,
but remember that there are parvocellular and magnocellular ganglions.
Just wanted to clarify...Are rhodopsin found on rods, as well as
cones?
(In the website notes, it only mentions rhodopsin located on the
discs of rods, not around the invaginations of cones, which Prof. Olavarria
drew in his diagram in class.)
Dr. Olavarria did mention Rhodopsin being
located on both rods (discs) and cones (invaginations) in class.
Could you explain the case of LM?
LM was an example of a patient with a lesion in
a particular portion or the Parietal Cortex. Her deficeit was in
the perception of movement. She could see, but couldn't see moving
objects. This outlines the importance of the separate processing
pathways in generating a representation of our world.
How does the vertical meridian (VM) and horizontal meridian (HM)
divide vision?
The HM divides our vision into upper and
lower fields. It is simply the point at which the visual field is
in the exact middle. The VM is the most lateral (toward the side
of the brain) boundary of the primary visual (striate) cortex. This
essentially separates the visual world into the right and left sides.
These demarcations are necessary mainly because the visual field (retinotopic
map) is completely backwards in this representation.
When regarding vision, what does it mean to say you have a deficit
due to a lesion? What is a lesion?
A lesion is a generic term for brain damage.
This could be due to a stroke, physical injury , or a myriad of other causes.
When does monocularity occur for the first time? In what layers
does it occur?
Monocularity is present in every levelof
the visual system through layer IV of the primary visual cortex.
The projections from here converge in layers II and III and these are the
first binocular representations of a visual stimulus.
In the visual system we talked about how images recieved by the fovea
are magnified. Do we actually see these things as larger in relation
to other objects, or do we only see them in greater detail?
We see them in greater detail. The "magnification"
occurs since we have a much larger area of visual cortex allotted to the
fovea compared to peripheral areas of the retina.
Does area V1 (V-one) have 6 layers?
Yes, but please do not confuse "V1" with
VI (V-one with six). Area V1 or Primary visual cortex is commonly
called striate cortex. The six layers are arranged inside out (I
near the pia matter and VI farthest from the skull). Projections
from the dLGN synapse in layer IV, and go to the other layers from there.
How do the 6 layers of neurons correspond to the lobes? (which layers
are in which lobes?)
Dr. Olavarria mentioned that all areas of
cortex (lobes of the brain) have these six distinct layers.
What is ataxia?
Ataxia is "an inability to coordinate voluntary
muscle movements". The visual system is important for the guidance
of movements so a Parietal/occipital lesion as seen in Balint syndrome
can result in a form of ataxia.
What is ocular apraxia?
This is an inability to scan and fixate on objects
properly. The term apraxia is often used in respect to skilled motor
acts so you can see how it equates.
Could you please explain how the dLGN in the Thalamus is monocular
and its relationship with the ganglion cells from the retina.
In class Dr. Olavarria drew up a diagram showing
how the retinal ganglion cells project to particular layers of the dLGN.
Even though axons from the nasal portion of the eyes have crossed over
to the contralateral side by this point they innervate separate, alternating
layers of the dLGN. These populaions of nuerons are monocular since
there is a distinct separation between input from each eye at this level
of the visual system.
What are the names of the ossicles and the specific functions of
the middle ear?
The ossicles are the small bones in the ear, but
please don't worry about their names unless Dr. Olavarria says otherwise.
They are connected to the ear drum which vibrates them at a rate equal
to the frequency of the sound. The last ossicle vibrates the oval
window, and this creates a change in the fluid pressure of the ear at a
rate equal to the frequency as well. In a sense the ossicles simply
transfer the sound waves between membranes, but your book also mentions
that they "amplify" the signal since it takes more pressure to compress
the fluid in the ear than it does to compress air.
Prof. Knight mentioned a) Impedence matching and b) Acoustic reflex
- but I didn't get the details on these two pertaining to middle ear functions.
Dr. Knight did not focus on impedence matching
at all so I do not believe that you will have to know it. The acoustic
reflex is essential in that the muscles supporting the ossicles are able
to contract and essentially protect them from damage due to loud sounds.
This is also important for protecting our ears from the relatively loud
sounds that we produce when speaking.
What is transduction in regards to the auditory system? When cillia
move, is a potential generated by the cilial cells, or does some neuron
perceive the movement and react with a potential of some sort?
Transduction is the conversion of a physical
stimulus into electrical changes that the brain can work with. When
the hair cells (cilia) connected to the basilar mambrane move in response
to particular frequencies they open ion channels that can ultimately affect
the firing rate of auditory neurons.
What is the function of the basilar membrane?
The cillia are imbedded in the basilar membrane.
Movements in this membrane are produced by sounds and this is the basis
for pitch perception, discrimination, and transduction.
For human hearing range, do the waves need
to be at high intensity, and relatively low hertz?
Not exactly... at low frequencies it appears that
the sounds must be at high intensity, but in the most common range of frequencies
our hearing is quite sensitive and does not need high intensity stimuli.
What is the approximate intensity range in
which humans can respond to 0 decibels?
We are most sensitive to frequencies in the
1,000 to 4,000Hz range. From the graph it appeared that we could
respond to very weak sounds in this range. Please remember that the
decibel scale is not absolute, and that 0 dBels or less above a frequency
of 1000Hz is not actually "negative sound levels". This is slightly
confusing, don't lose sleep over the minutae.
What keeps the bones in the inner ear from moving around during normal
movement of the head?
A movement of the head would presumably be at a
rate that would be slow enough (less than 20 "shakes"/sec) so as not to
be mistaken for sound.
What are the scala vestibuli and the scala tympani?
These are the separate channels of the cochlea
in which the waves of sound travel through the viscous fluid of the inner
ear.
Visual System, Auditory System
What are the specific functions of the inner hair cells?
We did not focus on their function at all, just
worry about the outer hair cells.
Is the air in the outer ear and the liquid in the inner ear compressed
at the same time?
The air is compressed, but the fluid in the cochlea
is simply disturbed since it would actually take a tremendous amount of
force to compress a liquid. Yes, this compression of air and disruption
of the fluid happens at exactly the same frequency.
What does tonoptically organized mean?
This means that similiar frequencies are
located next to each other on the basilar membrane. We did not get
to a point in the lecture where we talked about this level of organization
in the cortex.
What do optic radiations do?
This is just a fancy term for the axons that project
from the dLGN to Layer IV of the striate cortex. Don't let the terminology
throw you off.
Can we please go over the action potential in the auditory system
again?
We were given a lot of information about auditory
transduction, but didn't quite get to the production of action potentials.
You know that the sound waves eventually end up moving the outer hair cells
against the tectoral memebrane. This physical movement directly opens
ion channels by themselves. We need not get more specific than this
for now since we know that a change in membrane potential (regardless
of direction) can affect the rate of action potential firing, and ultimately
lead to coded information reaching our cortex.
What are complex waves regarding hearing?
The bottom line is that it is rare to have a pure
tone vibrating our tympanic membrane. We have a highly develpoed
auditory system that is able to discriminate very well given the complex
composition of the sounds reaching our ears.
What is the difference between frequency, intensity, and velocity?
Frequency is the periodicity, or distance between
peaks of the sound wave creating pitch. Intensity is the amplitude
or vertical size of the wave perceived as loudness. Velocity is fairly
constant for our purposes... don't worry about it too much.
Will you explain occular dominance?
This was not covered and won't be on the
test.
What is the difference between the round window and the oval windows
of the ear, and what are their functions?
The oval window vibrates in response to movement
of the ossicles. Since this is causing a disruption of the fluid
in the rigid cochlea, the movement must be absorbed somewhere. The
round window moves in an exactly opposite and equal fashion to keep the
system intact.
What part does Ca++ play in visual transduction and dark current?
Ca++ is always necessary for neurotransmitter release.
With the slight depolarization of the membrane associated with dark current
we have the influx of Calcium and release of inhibitory neurotransmitter
by the receptors.
What is the difference between distal and proximal stimuli in hearing?
The distal stimulus is the sound wave as it passes
through the air. The proximal stimulus is the resulting disruption
of the fluid of the cochlea.
What is impedance matching?
I think of this as having the tympanic membrane
and the oval window vibrating at exactly the same frequency.
Is the tympanic membrane the ear drum?
Yes, they are one in the same.
What determines the pitch perception in our hearing?
Different portions of the basilar membrane respond
to different frequencies. Higher frequencies near the base, and lower
frequencies toward the end farthest from the oval window.
Please explain D-bells and hertz measurements. It sounds like both
are sound waves that the ear hears, but I don't understand the difference.
Is there a plain English translation?
They are two separate components of a sound wave. Decibels
refers to loudness, or the intensity of a sound. This can be seen in the
amplitude of the sound wave. Hertz is the frequency of the wave.
We hear different frequencies as separate pitches, and changes in decibels as
a difference in loudness.
Where are the hair structures in the inner ear located?
They are located on the organs of corti on the basilar membrane.
Don't forget about their connection to the tectoral membrane as well.
How do compression and rarefaction work in the hearing process?
Compression and rarefaction refer to the density of air molecules
as a wave of sound is transmitted.
Where exactly is the retino-hypothalamic tract and the function of
the SCN?
This tract is simply a few axons branching
off from retinal ganglions as the pass through the optic chiasm.
These axons synapse on the SCN (suprachiasmatic nucleus) and provide the
input necessary to reset the circadian clock. One role of the SCN
is to regulate melatonin production in the Pineal gland which can make
us sleepy.
What does endogenous mean when talking about endogenous cycles?
This term simply refers to something that is produced
in the body. "Exogenous" is something produced artificially.
What is the definition of a free-running rhythm?
This is an artifically produced instance
where a subject (human or animal) has no zeitgeiber to reset the circadin
clock each day. It this situation they rely solely upon their internal
clock which generally runs in cycles greater than 24 hours.
Why is the biological clock set on cycles that are slightly longer than
24 hours?
I don't know exactly. It would seem to me to be evolutionarilly
advantageous to have an ability to adapt to changing conditions. This
would require a "resettable" circadian clock. It also seems as though
our bodies "prefer" to shift backward so at least be thankful that it isn't
23.5 hours long.
How is it that baseball teams did better going west than east?
Presumably (this is a correlation and doesn't necessarilly
indicate causality here!), the teams traveling east have their lives more disrupted
since it is much harder to shift your sleep cycles forward. The shift
back a few hours when travelling west is more natural since we have a circadian
clock that is closer to 25 hours anyway.
Could you explain synchronization and non-synchronization as they relate
to brain waves?
Your book gives a really nice explanation for this
one on p. 253 (new ed.). Basically, when you are awake there are many
different brain regions firing at different rates and with different levels
of activity. In this awake state the activity is rather random based on
our "crude" EEG measurement. This type of instrument provides excellent
temporal resolution (accurate detection of changes in activity over time), but
very poor spatial resolution (you can't detect changes in areas the are near
to each other). The net result is an EEG reading that has dis-synchronous
low amplitude waves. During the deep stages of sleep the numerous, random
firings disappear and the remaining waves are produced by processes that evoke
activity in a synchronized fashion. Don't ask me how that actually occurs.
When brain waves are measured (EEG) what exactly are we reading? Is
it an electrical impulse in the brain?
The EEG measures electrical activity in the brain.
Basically, it is an output on a grand scale of all of the action potentials
that it can read within the detectable range of each individual electrode.
If you wake up in the middle of the night and go back to sleep do you start
over at stage 1, or say if you were in stage 3 do you return there? And
even if you don't return right away, would you generally return to the stage
you were at a faster rate than before?
You can skip through stages of sleep (i.e. from 1
to 3), but my impression is that you cannot go directly from being awake to
stages 3 or 4. You will always start at stage 1 from an awake state.
What does it mean that dreams run in "real time"?
Your book mentioned experimental data supporting the
notion that a subject's dream subjectively lasts for about the same amount of
time as REM. Meaning... if your dream sequence lasts 10 minutes in your
mind it most likely lasted approx. 10 minutes in reality.
In what stage does dreaming occur?
Dreaming can occur in all four stages of sleep, but
it is most common, vivid, and lasts the longest during REM.
Why is circadian theory thought to be more accurate than recuperation theory?
This is convention since the available data do not
support the recuperation theory very well. When we work very hard we do
not necessarily sleep longer. Also, animals that work much harder (horses
for example) do not necessarily sleep longer than animals that are relatively
lazy (sloths). The circadian theory (evolutionary) seems more accurate
when you correlate the number of hours slept and the level of vigilance necessary
for the animal to protect itself from predators. Both sides will admit
that there is some truth to both positions, however. So don't go home
thinking that wither one explains everything.
How long does it usually take for a person to reach the REM stage?
Your book says that it takes approximately 60 to 90
minutes to begin coming back up toward REM sleep after you first fall asleep.
The graphs in your book also show about 2 hours between REM sleep stages throughout
the night.
Could you explain the "REM anomaly" Dr.Olivaria mentioned in class?
The original discoverers of REM called it "paradoxical
sleep" since it resembled the deepest stages of sleep with regards to muscle
tone, but your eyes appeared to be in their most active state during this stage
of sleep. This would seem to be a little anomalous.
Why do we go in and out of stages of sleep? Why don't we just stay
in REM for a long period of time?
We actually know VERY LITTLE about what is
going on during sleep. It appears that different brain regions, and different
learned patterns are being reinforced and activated in other stages of sleep
as well. Some researchers are indicating that slow wave sleep can be just
as important as REM for memory consolidation. It would appear that REM
is the most important part from what we have learned, but I would caution you
on being too narrow here.
How many times during one night can/do people go from stage 1 to 4 and vice
versa?
This can vary from person to person, and from night
to night for any given subject. The estimates that I have seen indicate
something on the order of 4 to 6 cycles on average.
What does it mean when an alpha or delta wave have high amplitude?
Just like the physical properties of sound and light
waves, the size (vertical height) of a wave is its amplitude. For sound
we call this loudness, and for light we called this brightness.
When you wake up tired, either due to not enough sleep or to being up earlier
than normal, why do you still remain tired throughout the day? Also... I wasn't
quite sold on the idea that we don't lose cognitive abilities when we loose
sleep. I know that I don't do homework very well when I'm tired.
Is this really contradictory?
Everyone responds differently when their normal cycles
are disrupted. The tired feeling that you experience may reflect this
disruption, rather than actual deficits produced by lack of sleep. To
a certain extent we DO NOT perform as well if we are sleep deprived.
You can find a noticeable difference in reaction times and in sensitive cognitive
tests. The bottom line is that we do not perform so poorly that it justifies
that recuperation theory of sleep.
Does the amplitude continue to increase just through the four stages or
through the emergent stage as well?
The amplitude of the waves increases as you go from
stage 1 down to stage 4. As you cycle back up toward REM sleep the amplitude
of the waves decreases and the frequency increases.
Can you be paralyzed as in REM sleep but semi-conscious at the same time.
I was once sort of conscious, but could not move my body at all. What stage
is that?
This has been known to happen. At this point a person
is beginning to wake up, but the processes actively eliminating muscle tone
during REM are still working. It is very important that your muscles be
inactive during REM so you don't hurt yourself. Some people do not have
this occur and can get into trouble with their spouse! It can also be
problematic if you are still "paralyzed" as you begin to wake.
Are there other hormones that work similar to melatonin and increase drowsiness
in humans? For instance, like the sleep aids you buy, do those have melatonin
in them in order to induce sleep?
Many sleep aids are drugs that contain addictive sedatives.
These do not mimic natural hormones and can seriously disturb your sleep patterns
with chronic use.
Re: different sleep stages and EEG measurements - alert wakefulness brain
wave activity is measured at 13-30 Hz: How does this relate to our hearing
range of 20-20,000 Hz?
Hertz is a measurement of cycles per second in ANY
WAVE. One cycle per second = 1 Hz
Do other animals dream? If not, than why do we think this evolved
as unique to humans?
Anyone who has a dog will know that they like to growl,
whimper, and try to move when they are sleeping. This would seem to indicate
that they are dreaming to me. All animals (including humans) may need
REM sleep to reinforce events that were learned during the day. Humans
may have more elaborate or involved dreams, but I do not think that they are
all that different qualitatively.
In class, the Prof. said that sleep coincides with a lowering of the bodies
temperature. He also said that when you are sick and have a fever, your
body needs more sleep. This does does make sense?
This does make sense if you are careful to remember
that your need for sleep when you are sick may actually have nothing to do with
lowering your core body temp. You most likely just need more sleep to
help out your immune system.
What was meant by 'loss of muscle tone' during sleep?
During REM sleep you are unable to move portions of
your body other than your eyes and I think some rudimentary facial twitches.
"Muscle tone" is a generic term for having control over, or being able to contract
muscle fibers. This is related to having "toned" muscles from regular
workouts, but it is not exactly analogous. Without muscle tone you experience
a sort of "paralysis".
Why don't the 4 stages of sleep have to go in order (ex. 12341234)- why
isn't the progression always the same?
The stages ARE in order. They basically
go 1 2 3 4 3 2 REM 2 3 4 3 2 REM. It would be difficult to go from stage
4 directly to REM sleep as your initial ordering suggests. Sometimes,
stages are skipped... but they always go in relatively the same order.
Is sleepwalking/sleeptalking limited to any specific stage of sleep?
I believe that it occurs most frequently in stage
4, but don't quote me on that. It definitely doesn't occur during REM.
Is the emergent stage 1 just "stage 1" (initial stage) repeated over again?
No, it appears only when we initially fall asleep.
When we cycle through the stages and reach stage 1 again it is actually REM
sleep. REM is similar to stage one in some characteristics, but it is
only in REM that you get the Rapid Eye Movements, loss of muscle tone, and a
preponderance of dreaming.
When are we in the "alert wakefulness" stage of sleep? When we first
get in bed and close our eyes?
Basically, Yes.
Other than those listed in class notes, what are some other zeitgebers that
can reset our 'master clocks'?
The main thing that we focussed on was bright light.
Aside from that I am unaware of any significant others.
Is the term "Biological Clock" the same as the term Circadian rhythm/cycles?
Yes, we use "biological clock" in popular terminology.
It is easier for the public to remember.
What determines our body weight set point (or settling point),
is it entirely genetic? What about greatly obese people - I don't think
that their bodies are at "equilibrium"... is it then virtually impossible to
lose weight because you always return to what you were before?
Genetics most likely has a lot to do with it, but many environmentat
factors play a role as well. I would argue that a lifetime of regular
exercise could modify or attenuate a genetic predisposition to being a little
over weight. The bottom line is that your body works very hard to maintiain
its "settling point", and it will resist any attempts to maintain a weight greatly
above or below it. Dr. Olavarria outlined the parameters by which a person
could acheive a lower settling point with a reduced calorie diet, but once you
increase your caloric intake back to the previous levels your body will bounce
back to the old settling point. For those with a particularly "stubborn"
body... it may just be best to be happy with yourself the way you are.
What makes your set point change at different points in your life?
Why is it harder to lose weight the older you are?
Different levels of caloric intake, exercise, and metabolism
can affect your set point (settling point). Older people are generally
less active than you youngsters, and have a slower metabolism to boot.
Since the lipostatic theory says that our body tends to regain its normal
amount of fat if we stop dieting, is it more healthful to maintain that fat
instead of losing it?
It depends on how much fat you are talking about... as you
may very well imagine, a person who is very overweight should try to lose that
fat and keep it off. Someone who is simply five pounds overweight may
put themselves through undue stress by constantly dieting to lose it.
When a person diets they often lose important muscle mass, this can be
very detrimental if your goal is to continue burning calories after the diet
is over.
Can you explain the rat experiment about the caloric content of food?
Rats are VERY good at maintaining a relatively healthy body
weight. In these experiments the researchers reduced the caloric content
of the rat's food. In other words, they put in fillers that didn't provide
as much nutrition as the rat needs on a daily basis. Without having any
"conscious" knowledge of the situation, the rats increased their food intake
to provide the extra calories that they need. This illustrates the presence
of feedback mechanisms that can affect food intake independent of the amount,
or bulkiness of the food that is eaten. When the nutritive value of the
food fell below 50% the rats lost weight, regardless since they could not put
any more of the bulky food into their distended stomachs.
How would the body be able to monitor/measure glucose utilization? That
sounds very very complicated, much more so than monitoring the blood-glucose
level.
The specific mechanisms are indeed complicated and ill defined.
You are right when you say that it would seem to be easier to monitor the blood
glucose level, but the question is... is that the best way to maintain homeostasis?
Blood sugar (glucose) levels can rise and fall quickly over the course of a
day. They can also be abnormally elevated for diabetics even though they
aren't utilizing most of it. In extreme cases, glucose is even elimintaed
through the urine I believe. To me it seems as though there is not always
a well defined ratio of glucose that is stored/utilized/lost in all situations,
and for all people. It is the actual utilization and conversion of glucose
that actually matters to the body, and in monitoring this rate it has a much
more accurate reading of the body's immediate energy/caloric needs.
What is lipectomy?
This would be the surgical removal of fatty tissue (lipids)
with a scalpel as opposed to sucking it out with liposuction. The take-home
message is that without a change in diet to accompany the surgery, your body
will work to replace the fat that has been removed, and that person will have
to pay another 5 grand visit to the surgeon in a few more months.
Are the glucostatic and lipstatic theories both used or does one have precedence
over the other?
Dr. Olavarria mentioned that they are both used, and that
they basically work in harmony. Glucostatic mechanisms seem to modify
and/or monitor food utilization on a daily basis. Remember... glucose
is burnt quickly and stored as fat rather quickly. The lipostatic mechanisms
are more for long term maintainance and regulation of our fat stores.
Basically to make sure that we could survive a food shortage is need be.
What does "the incentive value of food" mean?
When you talk about a theory of ingestive behaviour,
it is important to think about the social aspects of eating as well. This
"incentive value" has been introduced to add some flexibility into the theories,
and to better explain both human and non-human eating behaviors. Rats
that are given a wide variety of interesting foods to try will tend to over
eat even though they are generally so good at regulating this behavior.
Remember the "cafeteria style" idea. Humans tend to overeat around the
Holidays becase of all the great choices, and the social importance of sharing
these extended meals with family. We do not pretend to think that it is
only mechanical/physiological processes that regulate eating behavior.
Many pychological processes contribute to the DECISION to eat, or eat more food.
Anorexia is a psychological disorder that can affect eating behaviors independent
of the body's physical mechanisms affecting hunger and satiety.
Also regarding the "Leaky Barel" model...why would overeating increase leakage
and therefore energy expenditure? That doesn't seem right. Increased eating
should have an effect on storage, not expenditure. Right?
Not exactly... An increase in eating would increase storage
for a little while, but after you reach a slightly higher "settling point" you
will burn all of the excess calories and will not continue to store extra fat.
My understanding of this situation is that the body has a certain amount of
flexibility in the efficiency with which it burns calories. I there is
an abundance of excess calories the body tends to be inefficient, but when you
are on a diet... your body will become very efficient and store as much of the
available calories as possible (resisting CHANGE here again). It would
seem that the body has the ability to metabolize pretty much all of the calories
that you eat... it is just too bad that we can't communicate with it to let
it know that we aren't starving, and that it wouldn't be a bad thing to lose
a little bit of the extra fat that is stored in case of emergency.
Can you better explain the 3 phases of energy metabolism, especially the
cephalic phase?
The three stages are "cepahlic", "absorptive", and "fasting".
The cephalic stage encompasses all of our eating behavior. Remember...
cephalic literalliy means of or relating to the brain. During this phase
you see and smell food, become motivated to eat, seek out food, and actually
eat it completely. During the absorptive phase you do two things: burn
glucose for immediate needs, and convert all excess glucose to lipids for storage.
During the fasting stage you are simply using up stored energy reserves.
Insulin is released in the cephalic and absorptive phases. Glucagon is
released during the fasting phase.
When, or what, inhibits glucose utilization AND converts glucose to glucagon
AND converts fats to fatty acids (is this storage?) for energy (storage or expenditure)?
Is this insulin?
This is a VERY CONFUSING QUESTION, so I would advise you
to please study this information in a different way. There are two main
hormones here, and they both work together to produce all of these effects.
Insulin is produced when blood sugar levels rise in order to promote utilization
of glucose and its conversion to lipids for storage. Glucagon is
the exact opposite of insulin. It is released when blood sugar is low,
and promotes the utilization of stored fats and glycogen for energy.
What should we remember about the VMH and LH for hunger and satiety?
If you want my opinion I think you should study the
chart well enough to reconstruct it during the test so that it can aid in answering
potentially tricky questions. Experiments showed that exciting the LH
caused rats to over-eat, and that lesioning it made rats stop eating.
If you remember either one of these points you have enough info to make the
graph. When you are looking at your notes please remember that the Lateral
Hypothalamus and the Vental Medial Hypothalamus work EXACTLY OPPOSITE from each
other. Also, make sure you can generalize enough to see that a rise in
glucose/fat levels would inhibit the LH to produce satiety, and that this feeling
of satiety is what the rat experiences when the LH is lesioned and the rat loses
weight in an experiment.
How do set point and settling point differ? What does it mean that "there
is no set point defined" for the settling point?
Originally researchers talked about a "set point" that everybody
had. This was a fixed and inflexible figure that everyone's body worked
to stay at. This original theory was modified since it became obvious
that this point could change. It has been termed a "settling point" because
even though your body strives to maintain this weight, it can be changed to
a new "settling point", which your body will stay near given new environmental
conditions (caloric intake, exercise, etc.).
Can you explain the experiment where the stomach was "cut" smaller and the
"new stomach" was attached directly to duodenum?
The take-home message is that with a smaller stomach a person
has a reduced capacity to digest large amounts of food at any given time.
This forces a person to eat smaller, less frequent meals throughout the day.
Incidentally, this is what many people suggest for everyone else as well.
I did not understand the "balloon test". What did swallowing the balloon
prove? Was it inflated to stop them from being hungry and then deflated
to make them hungry?
Yes, and yes. When the balloon was inflated in a rat's
stomach it stopped eating. This outlines the importance of the feedback
that the distension of the stomach provides for injestive behaviors. However,
it is important to remember that this type of feedback is not the only mechanism,
since we saw the importance of food content in the rat experiments using reduced
calorie food.
What happens to people when their gall bladder is removed and they no longer
have the ability to emulsify fats? Is there a back up system? Would
they lose weight? Does their lymphatic system get clogged with fat particles?
I am slighty unsure of the specifics, but they definitely
have to modify their diets and take supplements to avoid large amounts of fat
in their diet. If a patient does this properly it would seem logical to
think that they would lose some wieght as well.
Could you explain how adenosine works with the wake and sleep cycle?
The release of adenosine makes you sleepy since it inhibits
the body's arousal system.
How does caffeine interact with adenosine?
Caffeine inhibits adenosine, so
you have stimulation of the body from negative disinhibition (removal of an
inhibitory influence).
What does satiety stand for?
Satiety, or to be satiated simply means to be full
or appeased.
Can you please go over the process of hypovolemia again... with the antidiuretics,
aldosterone and the kidneys?
Dr. Olavarria will spend some more time on this for
Wed, but I can touch on it now. Hypovolemia is a reduction in blood volume.
The Baroreceptors in the wall of the Heart can detect a change in blood pressure,
and the blood flow receptors in the Kidneys detect a loss in blood volume as
well. Activation of these receptors leads to a release of ADH (antidiaretic
hormone) and vasopressin. Dr. Olavarria's chart at the end of class on
monday showed an increase in Renin production with stimulation of the blood
flow receptors in the kidneys. This led to an increase in angiotensin
II production which increases blood pressure, this also stimulates an increase
in aldosterone production to help save Sodium in the Kidneys. This just
adds a little bit of complexity to the system that he mentioned earlier in class,
and does not pose a huge conceptual threat for us.
Which plays the biggest role in the regulation of eating for the leaky barrel
model? The amount of sugar, fat, or social learning?
The most important part of the model is the body's
adjustment to an increased caloric intake. Regardless of what kind of
food, or the reasons why it was injested, your body will adapt and form a new
set point in the face of intake/expenditure changes.
Dr. Olavarria talked about different ways in which osmosis occurrs.
How many were there and what were they briefly.
Just think of osmosis as a single process allowing
water to pass relatively freely through the cell walls in response to a change
in tonicity. Dr. Olavarria spoke about different types of tonicity, but
not different types of osmosis that I can recall.
Do we always use our fasting phase of metabolism or is it only when we actually
fast?
The fasting phase is invoked all of the time, not
just when we go on a long fast. Every night your body runs out of food
and must resort to stored energy to make it through to the morning meal (break
the fast). This can also happen between meals during the day since the
glucose that is ingested will only last for a short period of time before the
conversion to fat begins.
Could you please explain again what causes water to leave the cell when
the EC fluid is hypertonic. I am confused because to me "hypertonic" indicates
that the EC contains more (water?) than the IC fluid. According to the
concentration gradient, doesn't this mean that water will go into the cell?
Or does hypertonic refer to the salt content?
Hypertonic refers to an increased salt content.
That means that osmotic pressure would tend to push water toward a concentration
of increased tonicity, or increased salt content.
What is the role of the hypothalamic osmoreceptors in thirst?
Osmoreceptors have been shown to fire when in the
presence of a hypertonic solution/environment. This stimulation produces
drinking behaviors in rats, and promotes the release of ADH and Vasopressin.
Will you explain where the receptors for eating and drinking are located
in the hypothalamus.
Dr. Olavarria mentioned receptors for eating in the
LH (Lateral Hypothalamus) and the VMH (Ventromedial Hypothalamus). Stimulation
of these two produces opposite effects. The receptors for thirst that
we have been speaking of are located in the LH and the Lateral Pre-optic area
of the hypothalamus. Stimulation of these two areas appears to have the
same effects.
Is the set point theory for drinking similar to that of eating?
In the overall constuction of the basic concepts...yes.
What is the role of salts... Prof. Olavarria said that they are very important?
The concentration of salts in our bodily fluids determines
tonicity. This is essential for regulating the amount of water in the
body.
Do osmoreceptors fire when they meet water or is there another molecule
involved?
Dr. Olavarria mentioned that the cells increase their
rate of firing if a hypertonic solution was applied directly to them.
Whether or not another molcule mediates this interaction is beyond me.
Could you discuss the role of nuerotransmitters in satiety? Ditto for drinking?
For satiety we spoke of the role of CCK in producing
a signal in the presence of food. Knowing that it cannot cross the BBB
we hypothesized that it helps to indicate satiety through the distension mechanisms
of the stomach that already communicate with the brain, but I do not recall
Dr. Olavarria being too detailed in this account. For drinking we talked
about the stimulation of the LH and Lateral Pre-optic Area of the Hypothalamus
in determining cellular dehydration. We also learned about the role of
ADH (antidiaretic hormone) and Vasopressin (vasoconstricting hormone) in maintaining
blood volume and pressure, but have not talked about neurotransmitters with
regards to drinking.
When we discuss isotonicity and hypertonicity are we comparing things accross
time and subject or one or the other ( i.e. can something be hypertonic relative
to itself at a time in the past, and/or to another cell, amount of cellular
fluid)?
You are correct on all counts here. Remember
that the main reason for using hypertonic, hypotonic, and isotonic is to compare
one condition to another. It could be to a different area, or comparing
a condition to itself over a period of time.
Please explain the "Dual Center Set Point" model?
This indicates that both glucostatic and lipostatic
processes are important for maintaining the bodies energy reserves.
In regards to the dynamic and static phase in weight gain: a person can
gain 10 pounds over the Holidays..so theoretically it should be hard to lose
that "extra 10 pounds"....what does this have to do with body fat set points?
The increased caloric intake ove the Holiday season
can be enough to ellicit a shift in the body's settling point. Once your
settling point has been changed it is difficult to change it back, and requires
dilligence and a lot of work.
A final note to those who have
read this far, from Jake Kulstad, TA:
This class has really been a joy to TA. I have seen
many of you tackle this course with a lot of enthusiasm, and this has helped
to provide me with the energy that I needed to make it through the term as well.
Many of you have been continually challenging both me and Dr. Olavarria throughout
the class, and I hope that you don't lose that inquisitive spirit. This
was my first TA in Grad school, and you guys have made it a tremendously positive
experience for me. Thank you for all or your work, your never ending question,
and thank you for never simply accepting the answers that we gave you.
-jake