Neuroscience Review Questions
This is a huge collection of neuroscience review questions compiled from texts, old exams, etc. by a former graduate student at my university who was preparing to take her qualifying doctoral exams (thanks, Lynn, wherever you are).  If that's what you use these for, good luck!

Given a specific result in animal studies - what does it really show?
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.


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 Alzheimer’s 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


Distributed processing

Elementary brain operations

Language dominance of the left hemisphere

Mass action

Neuron doctrine


Serial and parallel processing



Amyotrophic Lateral Sclerosis


Conduction aphasia



Expressive aphasia

Head injury

Huntington’s disease

Muscular dystrophy





Receptive aphasia

Sleep disorders

Spinal cord injury


Tourette’s syndrome


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.


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 Brodmann’s 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


Small vs. large vesicles

Methods for removal of transmitter from the synaptic cleft

Precursors, mode of synthesis for the major transmitters


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?


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:
morphine nicotine

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?

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