What are advantages/disadvantages
of cell culture?
What are advantages/disadvantages of in
vivo studies?
What is the role of molecular biology in
neuroscience?
How can experience change structure? (include
development and maturity.)
How is Ca++ regulated?
Describe at least 3 roles/functions of
Ca++ in the nervous system.
Distinguishing characteristics of neuron.
Circuits vs. systems.
Functional brain imaging methods.
Excitotoxicity
Could feature detectors as complex as grandmother
cells account for how we recognize Grandmother?
What are the various signals and signal
transformations that neurons use to communicate?
What is cognition?
Instead of measuring intelligence with
IQ tests, should we use brain size, perhaps as measured by MRI?
What is Alzheimers disease?
What is known about its cause?
Based on what you know about human memory,
what advice would you have for students preparing for final exams?
Compare and contrast positive and negative
feedback in physiological systems, and give one example of each.
What are the morphological signs (at the
level of electron microscopy) of high levels of protein synthesis in a
cell? Describe the steps involved in protein synthesis.
Why does transcription of a particular
gene always lead to the same protein product?
Compare and contrast skeletal muscle and
smooth muscle.
Describe the general design of the nervous
system. Next, describe (in some detail) how communication takes place
between cells in the nervous system. Finally, describe the specializations
which make the nervous system unique among organ systems of the body.
Ontogeny recapitulates phylogeny?
What is the role of the neocortex?
What influences do sensory systems on neocortex?
Describe the processing of touch - (afferent
/ central processing / adaptation)
How has a given system changed over time?
Species?
Aggregate field view
Cellular connectionism
Cytoarchitectonics
Distributed processing
Elementary brain operations
Language dominance of the left hemisphere
Mass action
Neuron doctrine
Phrenology
Serial and parallel processing
ADD
Alzhiemers
Amyotrophic Lateral Sclerosis
Autism
Conduction aphasia
Dyslexia
Epilepsy
Expressive aphasia
Head injury
Huntingtons disease
Muscular dystrophy
Neurofibromatosis
Otosclerosis
Pain
Parkinsons
Receptive aphasia
Sleep disorders
Spinal cord injury
Stroke
Tourettes syndrome
Vertigo
Mysasthenia gravis
Understand the functional anatomy of the
human central and peripheral nervous systems.
Understand how new techniques help us explore
the functional anatomy of the human central nervous system.
Understand the major perceptual, movement,
and motivational systems of the CNS.
Understand the topographic arrangement
of sensory and motor representations in the CNS and the functional implications
of this organization.
Understand the historical development of
out current view of the localization of functional in the cerebral hemispheres.
Understand the principles of cellular connectionism
illustrated by the stretch reflex.
Understand the various signals and signal
transformations that neurons use to communicate.
Understand the genetic basis for the similarities
and differences among different types of neurons.
Understand the subcellular specialization
of the dorsal root ganglion sensory neurons and spinal motor neurons that
constitute the monosynaptic component of the stretch relex.
Understand the synthesis and fate of the
different classes of proteins that neurons express.
Understand the role of specialized transport
mechanisms within the neuron.
Understand the basic constituents of the
neuronal cytoskeleton and their role in determining neuronal structure,
in directing growth, and in axonal transport.
Understand how the myelin sheath around
the axon is formed by glial cells in the central and peripheral nervous
systems and its role in axonal conduction.
Cortex
Understand the different approaches of
experimental psychology, behaviorism, and cognitive psychology to the study
of behavior.
Understand the internal representations
and the five main approaches used in cognative neural science to analyze
them.
Understand how representations of personal
space are determined by the orderly mapping of somatic sensory inputs in
the cerebral cortex.
Understand how cortical maps can be modified
and the experimental for this form of learning.
Understand how the properties of the receptive
fields of neurons are used to analyze internal representations at cellular
level.
Understand how columns of cells in the
cortex form the elementary functional unit in the cerebral cortex.
Understand how lesions of the posterior
parietal cortex produce deficits in internal representations and the critical
role of the posterior parietal cortex in attentiveness.
Understand how knowledge of the basic cellular
mechanisms of neuronal function is invaluable in elucidating the etiology
of neurological disease.
Understand how clinical observation can
contribute significantly to our understanding of neuronal function.
Understand how the location and general
functions of the three main association areas of the cerebral cortex.
Understand how experimental tasks such
as the delayed response have been used to reveal the cognitive components
of the prefrontal area.
Understand the effects of lesions of the
parietal and temporal associateion areas on cognitive function.
Understand the main functions of each cerebral
hemisphere, how studies of patients with trans-sections of the corpus callosum
have revealed specialized functions in the two hemispheres, and how anatomical
differences between the two sides of the brain might contribute to hemispheric
specialization.
Understand parallel distributed processing
models and how they can be used to investigate cognitive functions of the
brain.
What is the association cortex?
What is consciousness?
Describe the functions of the parietal
association cortex, temporal association cortex, and frontal association
cortex.
What are the major inputs and output of
association cortex? Can you think of possible functions for each
of these connections?
How did Brodmann decide where to put the
boundaries between Brodmanns areas?
Which layer(s) of the neocortex specialize
in receiving inputs? In sending outputs?
What is contralateral neglect syndrome?
Why is it always the left side that is neglected?
What is agnosia (e.g. prosopagnosia)?
What are the different techniques or approaches
that have contributed to our knowledge of frontal lobe function?
Parietal lobe function?
What is the delayed reponse task?
What part of the brain is particularly critical for this task?
Where are the recognition neurons that
respond best to monkey faces?
A patient with damage to the frontal cortex
would have difficulty changing criteria in the Wisconsin card sorting test
- Why?
Instead of measuring intelligence with
IQ tests, should we just use brain size, perhaps as measured by MRI?
Outlined the key features of three historian
traditions: experimental psychology, behaviorism, and cognitive psychology.
For each tradition identify a strength and a weakness.
What is manned by an internal representation?
Identified two important contributions
of computer science to cognitive neural science.
Explain the difference between the methods
used by Marshall and Penfield for mapping the organization of the somatic
sensory cortex. Which method tells us more about conscious perception?
With respect to the modify ability of cortical
maps, what is meant by the statement, "cells that fire to gather, wire
together"?
Distinguish between the functions of the
premotor area and the prefrontal area of frontal cortex. Identify
the differences between the inputs to these areas and their outputs to
other parts of the brain.
List the parts of the brain that are considered
part of the limbic association cortex.
The most important function of the prefrontal
association area is to weigh the consequences of future actions and act
accordingly. Discuss how studies in monkeys using spatial delayed
-- response tasks are related to this function.
Discuss possible functions of the corpus
callosum, as revealed by studies of "split -- brain" animals and humans
in whom the corpus callosum has been surgically transacted.
Describe how sodium and amytal can used
to determine which side of the brain is dominant for language in a patient.
Identify the key differences between layered
networks and recover and networks. Which type of network to you think
might be a better analog of brain circuits responsible for long -- term
memory? Explain your answer.
Define what is manned by back -- propagation
in a layered network. Briefly describe how it works do you think
such a mechanism can account for development of connections in real nervous
systems? Explain your answer.
A new hereditary human disease is discovered
in which the primary symptom is muscle weakness, very much like myesthenia
gravis/patience with this disease have normal numbers of ACh receptors
at the neuromuscular junction as determined biochemically, and the junctional
specializations in the muscle membrane appear normal. Physiological
experiments on muscle biopsies indicate that the and played potential is
reduced in these patients. Quantitative analysis of the end -- played
potential in the biopsies indicates that the number of quanta released
is normal, but the size of the single quantal response and spontaneous
miniature end -- played potentials is similarly reduced. Propose
to alternative causes for the disease, one presynaptic in origin and other
postsynaptic in origin, and propose experiments it that can distinguish
between them.
Trace the transcerebral pathway of sensory
information leading from mechanical stimulation of the skin on a finger
to the coordinated movement of the finger in response to the stimulus.
If the optic chiasm is cut, what parts
of the visual field would be lost?
General topics:
Membrane potentials
Action potential
Postsynaptic potential (EPSP, IPSP)
Receptor potential
Ion channels
Ion pumps
Nernst vs. Goldman equations
Equilibrium potential
Ionic bases of the resting potential and
action potential
Usefulness of voltage clamp
Early and late currents in the action potential
TTX TEA oubain
Membrane conductance
Passive current flow
Role of myelination in conduction of electrical
signals
Refractory period
Usefulness of patch clamping
Molecular structure of voltage -- gated
ion channels
Properties of the Na+/K+ pump
Features of the neuromuscular junction
Compare features and advantages of electrical
vs. chemical synapses
Bases of MEPP, EPP
Evidence for recycling of synaptic vesicles
Evidence for role of calcium in transmitter
secretion
Proteins involved in transmitter release
Criteria for determining that a substance
is a neurotransmitter
Chemical nature of neurotransmitters: classification
Compare small -- molecule vs. peptide transmitters
Co-transmitters
Small vs. large vesicles
Methods for removal of transmitter from
the synaptic cleft
Precursors, mode of synthesis for the major
transmitters
Excitotoxicity
Evidence of neurotransmitter involvement
in psychiatric disorders
What is a reversal potential? How
is it measured?
Why it is a reversal potential 0 mV at
the postsynaptic muscle fiber in a neuromuscular junction?
How does determining the reversal potential
help to identify the ion species involved at a postsynaptic site?
What is shunting inhibition?
True or false: only if the reversal potential
is more positive than the action potential threshold is the effect of a
transmitter excitatory.
Distinguish between EPSP and IPSP
What determines the net effect of an EPSP
and an IPSP generated in neighboring regions of a neuron?
Described as precisely as you can the role
of a neurotransmitter receptor.
Define ionotropic receptor, ligand -- gated
ion channel, metabotropic receptor. G-protein coupled receptor, G-protein
Compare and contrast the action of metabotropic
vs. ionotropic receptors. What are the relative advantages of each?
Compare and contrast the structure of the
two major families of postsynaptic receptors.
Are GABAa receptors more similar to GABAb
receptors or to AMPA/kainate receptors?
What does each of the following do: a-bungarotoxin,
kainate, quisqualate, strychnine, and bicuculine?
What are the two main types of glutamate
receptors that are ligand -- gated ion channels?
What makes NMDA-type glutamate receptors
so exciting (especially to neurobiologists)?
What happens when GABAa receptors are activated,
and why does this generally result in inhibition?
Name some common drugs that act on GABAa
receptors.
What are the basis for myesthenia gravis,
and what approaches might be used to treat the symptoms?
Compare and contrast the two major second
passenger systems associated with metabotropic receptors in the nervous
system: 1) the cAMP system and 2) the phosphoinositide (PI) system.
List the main events that take place in each system.
Explain the relationship between channel
structure and function
Explain the selectivity of ion channels.
Describe the types and mechanisms of ion
channel gating.
Describe how drugs and toxins interact
with ion channels by competitive and non competitive interactions.
What is the genetic basis of channel diversity?
How can the patch clamping technique and
the reconstitution of channels in artificial bilayers be used to study
channel function.
How does the separation of charge across
the nerve cell membrane need to a resting membrane potential?
How does the selectivity of a variety of
resting ion channels lead to the overall selective permeability of the
cell membrane?
How to concentration gradients for violence
in combination with selective membrane permeability lead to the separation
of charge and thus to the resting membrane potential?
Describe the role of the Na -- potassium
pump in maintaining the ion concentration gradients across the cell membrane.
What is the difference between the equilibrium
model of the resting membrane potential for the glial cell (permeable only
to potassium) and the steady state model for the neuron (permeable to several
ion species but predominately to potassium).
Understand the application of the Nernst
and Goldman equations.
Understand the equivalent circuit model
for the resting neuronal membrane and its use in calculating V when Vm
is unchanging.
Understand the functional equivalents of
the membrane capacitance (lipid bilayer), conductance is (ion channels),
batteries (ion concentration gradients), and current generator (Na-potassium
pump) in an electrical equivalent model.
Understand how the resistive and capacitive
properties of neurons influence electrical signaling.
Understand the physical basis of the membrane
time constant and the length constant.
Understand how the membrane time constant
affects the conduction velocity of action potentials and the temporal summation
of synaptic potentials.
Understand how myelin increases conduction
velocity by reducing membrane capacitance and thus the membrane time constant.
Understand how the voltage clamp allows
study of the ionic mechanisms underlying the action potential.
Understand the gating of voltage -- gated
channels and the role of voltage -- gated Na and potassium channels in
generating the action potential in axons.
Understand the diversity of voltage --
gated channels, their molecular structure and relatedness, and their molecular
mechanisms of action.
Understand the similarities and differences
between the two types of synaptic transmission, electrical and chemical.
Understand the role of connexons in electrical
synaptic transmission.
Understand the similarities and differences
between direct chemical synaptic transmission via ionotropic receptors
and indirect chemical synaptic transmission via metabotropic or receptor
to tyrosine kinase.
Understand the role of each type of synaptic
transmission -- electrical and direct and indirect chemical -- in synaptic
plasticity and putting each type into behavioral context.
Understand the structure of the vertebrate
neuromuscular junction.
Understand the postsynaptic mechanisms
underlying the end plate potential.
Understand the relation between the and
-- plate potential and the end -- plate currents as measured under voltage
clamp.
Understand the concept of reversal potential,
especially as it applies to the end -- plate currents.
Understand the structure and function of
nicotinic ACh-activated channels and how their activity can account for
the properties of the and -- plate potential.
Understand the basic mechanisms of neuronal
integration: spatial summation, temporal summation, and the integration
of excitatory and in inventory synaptic input.
Understand excitatory and inhibitory synaptic
mechanisms and the transmitters usually associated with these activities
in vertebrates.
Understand the unique properties of the
NMDA receptor -- channel that make possible its role in synaptic plasticity:
voltage -- sensitivity, the ability to conduct calcium, and access to calcium/calmodulin
-- dependent protein kinase.
Understand the structural and functional
similarities and differences among resting (leakage channels), voltage
-- gated channels, transmitter -- gated channels, and gap -- junction channels
and their respective roles in determining neuronal activity.
How to neurons communicate?
Explain how they neurotransmitter could
effect the firing rate of a postsynaptic neuron solely by changing membrane
resistance.
Described on a cellular basis how neurotransmission
and can lead to changes in gene expression.
Describe calcium in the nervous system.
How is calcium regulated?
What makes calcium enter the presynaptic
terminal?
How do we know that calcium is necessary
for neurotransmitter release?
How does calcium initiate neurotransmitter
release?
What methods are used to prevent calcium
from entering the terminal?
Excitotoxicity.
How is patch -- clamping useful for determining
properties of receptors?
What is the role of myelination in conduction
of electrical signals?
Compare and contrast positive and negative
feedback in physiological systems, and give at least one example of each.
Compare and contrast electrical and chemical
synapses in terms of function, structure, and transmission.
Describe the Na/potassium pump.
Equilibrium potential.
Membrane potentials
Why is the Na equilibrium potential 55
mV but the peak of the action potential is 40 mV?
Membrane conductance
Passive current flow
What is a reversal potential? How
is it measured?
Why is the reversal potential 0 mV at the
postsynaptic muscle fiber in a neuromuscular junction?
How does determining the reversal potential
help to identify the ion species involved at a postsynaptic site?
Early and late currents in the action potential.
Refractory period.
Receptor potential
True or falls: only if the reversal potential
is more positive man the action potential threshold is the effect of a
transmitter excitatory.
Flood determines the net effect of an EPSP
and an IPSP generated in neighboring regions of a neuron?
Suppose you want to learn more about glutamate
receptors in the cerebellum. Describe a plan for your first experiment
using receptor binding.
Define association constant (Kd), and describe
two different ways to determine it.
What assumptions are made in choosing a
Scatachard analysis to determine Kd? What factors could be responsible
for nonlinearity? What types of approaches are used to determine
which of these factors is responsible?
What is nonspecific binding? How
is it determined experimentally?
Is it worthless to try studying a particular
receptor with a radioligand that binds to more than one receptor type?
Briefly, what steps are used to determine
the amino acid sequence of a receptor subunit? Can the sequence be
used to estimate which region is membrane spanning?
What does it mean to clone a receptor?
Would you expect the binding site for the
permeant ion ion in the aqueous for of a cation channel that allows the
ion to shed its waters of hydration to contain positively or negatively
charged amino acid residues? Why?
How would you determine the conductance
of individual ACh -- gated channels?
Certain ligand -- gated cation channels
allowed calcium to flow through them whereas difference but related channels
gated lithe same lake and do not. Alteration of a single positively
charged amino acid in a membrane -- spanning region of one of the channel's
subunit's renders that channel, which normally does not flux calcium, able
to do so. Provide a plausible explanation.
To drugs, A and B, bind relatively weekly
to a certain ligand -- gated channel, and of block its response to low
concentrations of the gating ligand. When the ligand is presented
in high concentration in the presence of each drug, the blockage of drug
A but not drug B is relieved. Explain.
All of the voltage -- gated cation channels
described (at the molecular level) to date all open in response to depolarization
and the drive from the same gene family but differ in their ion sensitivity.
What regions of the channel proteins would you expect to be conserved across
the numbers of the family and what regions would you expect to be divergent?
Suppose you penetrate a perfectly spherical
neuron with a current injection and voltage recording electrodes.
The resting membrane potential of the cell is -60 mV and it is 60 pm in
diameter (radius = 30 pm). Assume that, like most animal cells the
lipid bilayer of the cell has a capacitance of 1 pF per CM2.
Draw the equivalent circuit of the neuron
and electrodes, assuming it to have a passive membrane, and include the
membrane potential "battery." Label the components and identify which constituents
of the membrane give rise to the resistive and capacitive properties of
the equivalent circuit.
Compare the electrical and and chemical
properties of the nodal and internodal regions of a myelinated axon.
Included with your answer a diagram of a low -- magnification electron
micrograph of a longitudinal section through both regions.
What difference would you expect to see
in the distances between nodes in large and small axons? Why?
What alterations in the propagation characteristics
of axons would you expect in patients suffering from a demyelinated disease?
Explain.
Fast transient voltage -- gated potassium
channels (A channels) rapidly inactivate after activation by depolarization.
Using the techniques of molecular biology to alter jeans and produce mRNA
that can be expressed in cells, it is possible to make cells with A channels
missing various parts or having various other changes. A channels
produce from A channel proteins lacking the amino terminal end (some 80
amino acids in length) normally located in the cytoplasm we'll activate
normally but do not inactivate. If the first 20 amino acids at the amino
terminal end are removed, the same results is observed: no inactivation.
If the chain of amino acids following this initial 20 is shortened but
the initial 20 (henceforth referred to as the amino ball) are unaltered,
in activation occurs more rapidly than normal. If the chain is length
and but the ball unaltered, inactivation occurs more slowly than normal.
Alteration of positively charged amino acids in the ball to neutral amino
acids slows in activation. In mutant ball-less A channels that do
not inactivate, inactivation can be restored by injecting purified ball
polypeptide (i.e. 20 amino acid ball sequence) into the cells expressing
the mutant channels.
What do these experiments tell you about
the mechanism of in activation in A channels and its relation to in activation?
Removal of the intracellular loop between membrane -- spanning domains
III and IV of voltage -- gated Na channels likewise abolishes inactivation
without altering activation. Proposed a mechanism for inactivation
of these voltage-gated Na channels.
The method of using binding of radiolabeled
tetrodotoxin (TTX) to determine the distribution and density of voltage
-- gated Na channels in an axonal membrane in the textbook. How would
you expect the pattern to the different between myelinated and nonmyelinated
axons?
The interaction between voltage -- gated
Na channels and membrane potential is characterized in the textbook as
a positive feedback relation or regenerative. How would you characterize
the interaction between voltage -- gated potassium channels and membrane
potential?
The depolarization that occurs during and
action potential when voltage -- gated Na channels are opened spreads passively
to more open more voltage -- gated Na channels. The passive spread
of depolarization is bidirectional, but the action potential is propagated
in only one director. Why?
What effect would tetrodotoxin (TTX) have
on the production of action potentials? What effect would tetra-ethyl
ammonium (TEA) have on the production of action potentials? If either
condition would allow for the production of action potentials how would
the action potentials differ from normal action potentials?
You do a voltage -- clamp experiment in
the presence of hobbesisin. From the resting potential (-50 mV) you
issue a voltage step command to 0 mV. Draw the expected current through
voltage -- gated channels.
You do a voltage -- clamp experiment in
the presence of nanananabooboolin. From the resting potential (-50
mV) you issue a voltage step command to 0 mV. Draw the expected current
through voltage -- gated channels.
Compare electric synaptic transmission,
chemical synaptic transmission involving ionotropic receptors, and chemical
synaptic transmission involving metabotropic and tyrosine kinase receptors,
with respect to speed, duration, and behavioral function.
It is often said that the differences between
chemical synaptic transmission and endocrine function are blurry.
Explain.
Delineate the steps in the process of chemical
synaptic transmission from the arrival of the action potential at the presynaptic
terminal to the postsynaptic response.
How does the humorous expression concerning
human communication, "it's not what you say that masters, it's what ears
your audience has on," apply to chemical synaptic transmission.
how to the voltage -- gated axons differ
from the ACh activated channels of the vertebrates neuromuscular junction?
Escrine is a drug that blocks the action
of the enzyme ACE and the vertebrates neuromuscular junction. What
effect would you predict eserine to have on the amplitude of the end --
plate potential elicited by stimulation (depolarization) of the presynaptic
motor neuron at this junction? Why?
Describe how you would determine experimentally
the reversal potentials of an EPSP and IPSP.
Both nicotinic ACh receptor -- channels
and NMDA receptor -- channels are permeable to cations (mainly Na, potassium,
and calcium) and both mediate EPSPs. In what significant way to these
channels differ?
The voltage -- gated channels are made
up of polypeptides with four repeated segments with similar membrane --
spanning motifs or domains. (Voltage -- gated potassium channels
are composed of several, apparently four, subunits each with a single similar
membrane -- spanning domains.) Transmitter -- gated channels like
the nicotinic ACh channel are composed of five subunits, each with one
membrane -- spanning domain. Gap -- junction channels are composed
of six identical subunits, each with one membrane -- spanning domain. What
functional implications to the different numbers of membrane -- spanning
domains have for these types of channels?
Trace the synthesis and fate of a second
neuroactive peptide and and enzyme involved in the synthesis of a small
-- molecule transmitter (e.g. choline actyltransferase that synthesizes
acetylcholine from acetyl-co A and choline) from the site of productionof
mRNA in the nucleus to the site of transmitter/peptide release at a distant
presynaptic nerve terminal. How do the neuroactive peptides gets
into secretory vesicles for release at nerve terminals? How do small
-- while until transmitters get into synaptic vesicles for release and
nerve terminals?
How to second -- messenger systems amplify
receptor activation and impart flexibility to neuronal function through
their ability to both directly and indirectly modify channel function.
What is the role of G-proteins in mediating
the effects of metabotropic receptors.
What is the role of proteins kinases in
mediating the effects of second messengers on channel activity and cellular
metabolism.
What is the role of response element binding
finish proteins in mediating the effects of second messengers on gene transcription.
What is the role of presynaptic voltage-gated
calcium channels and calcium influx in synaptic transmission.
Describe the quantal nature of synaptic
transmission.
What all the the role of synaptic vesicles
in synaptic transmission.
Outlined the molecular machinery involved
in vesicles tethering, mobilization, and targeting to the active zone,
docking at the active zone, opening of the fusion for, and recycling and
refilling.
How do extrinsic and intrinsic factors
regulate transmitter release by influencing calcium influx in the presynaptic
cell and modification of the release machinery.
Describe the major small -- molecule transmitters,
there biosynthetic pathways, and there packaging into vesicles for release.
Describe the neuroactive peptides, there
synthesis as secretory polyproteins, and their processing and packaging
into vesicles by the endoplasmic reticulum and Golgi apparatus for transport
and and release.
What are the functional implications of
the different sites of synthesis of small -- molecule transmitters (by
cytoplasmic enzymes) and neuropeptide transmitters (as secretory polyproteins).
Describe the mechanisms for removal of
neurotransmitters from the synaptic cleft.
What is the difference between a neurotransmitter,
neuromodulator, neurohormone, and neuropeptide?
What criteria to you think should be used
to establish that a substance is a neurotransmitter? What methods
are commonly used to try to demonstrate these criteria, and what difficulties
are involved? To your criteria include newly discovered neurotransmitters
such as NO and CO, and do they exclude substances like growth factor worsened
that are not usually considered to be neurotransmitters?
Want is Dale's law?
What is the chemical nature of neurotransmitters,
and how are they classified?
Compare small -- molecule vs. peptide transmitters.
What are co -- transmitters?
Where is a given enzyme for a specific
neurotransmitter synthesis? Breakdown?
What are the precursors or a specific neurotransmitter?
What enzymes and neurotransmitters are
related?
What is the evidence for recycling of synaptic
vesicles?
Which proteins are involved in neurotransmitter
release?
What is the evidence for testicular release
of neurotransmitters? (Hint: include evidence from freeze -- fracture,
HRP and recycling in terminals, MEPP studies in the neuromuscular junction,
and co -- release of substances from adrenergic vesicles.)
What are the methods for removal of neurotransmitters
from the synaptic cleft?
Describe as precisely has possible the
role of a neurotransmitter receptor.
What are the four major classes of receptors?
Compare and contrast the structure of the
two major families of postsynaptic receptors.
Distinguish between "fast" and "slow" neurotransmission.
Define the following: ionotropic receptor,
ligand -- gated ion channel, metabotopic receptor, G-proteins coupled receptor,
and G-protein.
Compare and contrast the action of the
metabotropic vs. ionotropic receptor. What all are the relative advantages
of each?
Compare and contrast the two major second
messenger systems associated with metabotropic receptors in the nervous
system: 1) the cAMP system and 2) the PI system. List the main events
-- take place in each system.
Why is GTP (actually, a nonhydrolyzable
analog of GTP and sometimes) added in receptor binding experiments with
G-proteins coupled receptors?
What do autoreceptors do?
Briefly described how one could test whether
a receptor is an autoreceptor.
What are the main types of glutamate receptors?
What makes NMDA-type glutamate receptors
so exciting (especially to neurobiologists)?
Are GABAa receptors more similar to GABAb
receptors or to AMPA/kainate
Name some of the common drugs that act
on GABAa receptors.
How is ACh synthesized?
Briefly described the muscle ACh receptor.
Are all nicotinic receptors walked by Alpha-bungarotoxin?
Why is it difficult to determine which
receptor subunits constitute nicotinic receptors in the brain?
What are the subtypes of muscarinic receptors?
Are any of them ligand -- gated ion channels?
Biosynthetic pathways for catecholamines:
name the intermediates and enzymes. Which is the rate -- limiting
step?
What tricks can neurons use to regulate
the amount of norepinephrine according to demand?
How is the dopamine system affected in
schizophrenia? What is the main approach to treatment?
How is the dopamine system affected in
Parkinson's disease? What is the main approach to treatment?
What types of complications might arise
in trying to chronically manipulate the levels of dopamine?
In what respect all are B autoreceptors
a typical?
Where are most of the norepinephrine --
containing neurons?
What are two (of the three) major dopamine
cell groups?
What are the two main classes of dopamine
receptors, and what is the basis for this classification?
Activating a2 adrenergic receptors results
in what kind of second messenger systems response?
How is norepinephrine removed from the
synaptic cleft?
What methods have been used to identify
catecholamine systems in the brain?
Compare serotonin to catecholamines with
regard to load of synthesis, removal from the synaptic cleft, and relations
to vesicles.
How to neurons increase their level of
serotonin to meet extra demand?
What is the evidence for vesicular release
of serotonin?
What distinguishes one serotonin receptor
subtype from another? Which subtype is a ligand gated ion channel?
Describe the serotonin transporter's structural
and functional characteristics.
What is the difference between MAOI, TCA,
and SSRI antidepressants? Which of these includes Prozac? Is
serotonin implicated in any other clinical disorders besides depression?
What are the steps in synthesizing melatonin
from serotonin? How does like at night the press melatonin levels?
What brain nuclei provide the main source
of serotonin? The
Describe how opiate receptors were first
discovered.
Describe how endogenous opioid ligands
or first discovered.
What are the three main types of opiate
receptors? Name the category of endogenous opioid ligands preferred
by receptor type.
What his the second messenger outcome mediated
by opioid receptors?
What are the three main pre -- proproteins
that give rise to the major opioid peptides? What do these pre --
proproteins have in common?
What are some factors that may account
for the apparent mismatch between regional distribution of opioid peptides
and their receptors?
Describe the following:
8-OH-DPAT
a-bungarotoxin
amphetamine
apomorphine
atropine
bicuculline
blonidine
clorgyline
COMT
DAGO
deprenyl
d-turbocurarine
hemicholinium-3
isoprpteranol
kainate
MAO
morphine nicotine
muscarine
naloxone
naltrexone
nicotine
opium
phentolamine
prazosin
propanolol
quisqualate
reserpine
SCH-22390
spiroperidol
strychnine
vohimbine
How is it that GABA-ergic inhibitory motor
neurons and glutamatergic excitatory motor neurons in lobsters contain
equal amounts (concentrations) of glutamate?
What is meant by co -- transmission in
reference to synaptic transmission? Give an example.
What effect would intracellular injection
of the catalytic subunit of cAMP -- dependent protein kinase have on the
postsynaptic cells?
You have available a molecularly engineered
form of the regulatory subunit of cAMP -- dependent protein kinase, one
that lacks a cAMP binding site but retains its ability to bind with other
regulatory subunits and the catalytic subunits. What effect would
intracellular injection of this subunit have on the slow EPSP?
In chronically stressed animals, adrenergic
neurons increase their are levels of norepinephrine. Discuss the
mechanisms by which this stress -- induced increase may owe car.
Discuss ways in which the electrophysiological
effects mediated by metabotropic receptors differ from those mediated by
ionotropic receptors.
What are the four major systems involved
in movement control?
In what respect are upper motor neurons
not true motor neurons?
Define motor unit. Describe the differences
between different types of motor units.
Which type of motor unit predominates in
striated muscle's? Extra -- ocular eye muscles?
As synaptic activity increases, which motor
units are recruited last?
What symptoms result from damage to lower
motor neurons?
What are the two major ways of regulating
the gain of the stretch reflex?
Explain how gamma motor neurons regulate
gain.
Compare the roles of the Golgi tendon organ
and the muscle spindle in spinal reflexes.
Describe the activity in muscle spindle
afferents and Golgi tendon organ afferents when a muscle contracts or is
passively stretched.
What is the basis for muscle tone?
Diagram the flexion reflex and the crossed
extension reflex.
What is the evidence that central pattern
generators are important in locomotion?
Is descending control necessary to produce
the various gaits (walk, trot, pace, gallop).
Is sensory feedback necessary for walking?
Distinguish between the roles of motor
neurons in the medial vs. lateral parts of the ventral horn.
Distinguish between interneurons (intermediate
zone) that contact motor neurons in the medial vs. lateral parts of the
ventral horn.
What main role does each of these play
in motor control: vestibular nucleus, reticular formation, superior colliculus,
and red nucleus.
Do all of these project to the spinal cord?
Which cranial nerve supplies the semicircular
canals and otolith organs? What type of stimuli do they detect?
What and where is the reticular formation?
How it involved in the control of spinal cord circuitry?
Distinguish between feedforward and feedback
systems in postural control.
What are the two main subdivisions of the
premotor area? What is the role of the premotor area and how does
that differ from the role of the primary motor cortex?
Describe the route that axons from the
motor cortex take as they descend to the spinal cord.
What is the pyramidal tract? Where
are its neurons of origin and where does it terminate?
Distinguish between the uncrossed ventral
cortico-spinal tract and the crossed lateral cortico-spinal tract based
on origin, location, and function.
What did Kuyper's studies on monkeys show
for about the difference in function between the direct and indirect pathways
by which the motor cortex can influence the spinal cord? Which is
the phylogenetically newer pathway?
What is the upper motor neuron syndrome
and why is it important clinically?
What are the role of the cerebellum and
basal ganglia in the control of movements?
What are the two major sets of descending
motor projections and their major subdivisions?
