BioPsych Final

Mitochondria are concentrated at presynaptic terminals.

The endoplasmic reticulum is concentrated in axons.

Exocytosis and endocytosis are important for synaptic communication.

Glial cells rapidly transmit long-range electrical signals.

Both b and d

Golgi stain (light microscopy)

Extracellular electrical recordings

EEG (electroencephalogram)

Acetylcholinesterase staining

Electron microscopy of nervous tissue

They are technically easier to obtain.

They can be used in many more parts of the nervous system.

They can record synaptic and receptor potentials.

They can record from many neurons at once.

All of the Above

Diencephalon

Cerebellum

Cerebral Hemispheres

Spinal Cord

Brainstem

identify neurons expressing specific genes.

visualize the distribution of specific proteins in the nervous system.

trace anterograde pathways.

trace retrograde pathways

reveal structural changes associated with experimental lesions

Integrating information to assist neural computation

Maintaining the ionic milieu surrounding nerve cells

Hastening the propagation of neural impulses

Assisting synaptic transmission via neurotransmitter uptake

Providing scaffolds that assist neural development

Ease of genetic analysis and manipulation

Nervous systems of substantial complexity

An extensive and interesting behavioral repertoire

Specific neural structures or behaviors of interest

All of the above

Schwann Cells

Oligodendrocytes

Astrocytes

Microglia

All of the above

The visual world

Objects

Odors

Episodic Memory

Verbs and Nouns

It can be mapped by electrophysiological recording techniques.

It is characterized by a circular center and a donut-shaped surround.

It can involve an excitatory response (e.g., to touch).

It can involve an inhibitory response (e.g., to touch).

It is found only in primary sensory cortex.

dorsal root neuron

cranial neuron

afferent neuron

motor neuron (or motorneuron)

spinal interneuron

Zebrafish

Fruit fly

The nematode C. elegans

Mouse

The marine snail Aplysia

Peripheral

autonomic

enteric

sympathetic

parasympathetic

MRI

fMRI

PET

SPECT

CT

Every gene in the human genome is expressed in the CNS.

There are tens of thousands of neuron-specific genes (i.e., genes that are not expressed outside the CNS).

Most of the genes in the human genome are expressed in the CNS.

Humans have 100 times more genes than invertebrate animals such as Drosophila.

Humans have three to four times more genes than mice have.

Allesandro Volta

Luigi Galavani

Santiago Ramon y Cajal

Louis Pasteur

Thomas Hodgkin

mathematical ability

emotions

language

abstract thought

all of the above

MRI

fMRI

PET

SPECT

CT

represents convergent neural signaling.

represents divergent neural signaling.

represents massive neural integration.

must fire at very high frequencies to be useful.

can fire only at very low frequencies.

the Nissl stain

the Golgi stain

cresyl violet staining

fluorescence staining

electron microscopy

Nerve cells are exceptionally good conductors of electricity (much better than copper wires).

Nerve cells are similar in their electrical conduction properties to copper wires.

In comparison to copper wires, nerve cells are relatively poor conductors of electricity.

Nerve cells are unable to conduct electricity under any circumstances.

Nerve cells are electron sinks: they absorb many electrons, but no electricity comes out of them.

the Nernst equation is not able to predict potentials that precisely.

rapid fluctuations in membrane potential prevent accurate measurements.

the membrane has some resting permeability to species other than potassium.

potassium does not contribute to the resting membrane potential.

All of the above

Heat

Pressure

Sounds

Chemicals

Brain Waves

Nerst

ionic imbalance

Goldman

Finch and Augustine

atomic permeability

Potassium is higher inside cells than outside cells.

Sodium is higher outside cells than inside cells.

Chloride is higher outside cells than inside cells.

Calcium is higher outside cells than inside cells.

The total concentration of all ionic species is approximately the same for all nerve cells in all animals.

They can transmit signals over long distances.

They boost the spatial spread of electrical signals.

They are elicited by hyperpolarization.

They occur at threshold.

They are all-or-none.

100 mM K+, 10 mM K+

10 mM Na+, 100 mM Na+

10 mM Cl-, 100 mM Cl-

100 mM K+, 100 mM Na+

All of the above

positive charges bound to the inner and outer faces of

negative charges bound to the inner and outer faces of

movements of charged proteins within the plane of

fluxes of ions across

patterns of electrical eddy currents inside

Consumption of metabolic energy

Use of active transporters to create ionic gradients

Separation of large amounts of electrical charge, with excess positive charges stored inside the cell

Selective permeability of the cell membrane via different kinds of ion channels

Changes in membrane potential caused by the movement of ions across the cell membrane

the membrane potential approaches the Na+ Nernst potential during the rising phase.

the membrane potential approaches the Na+ Nernst potential during the falling phase.

sodium ions can move more quickly than other ionic species.

sodium ions are the only ions that can flow into the nerve cell body.

the sodium gradient explains the rising phase, falling phase, and overshoot of the action potential.

The large size of the axon makes it easy to penetrate with recording electrodes.

The axoplasm can be extruded, thus allowing studies of its composition.

Large synapses between giant nerve cells make them easy to study.

Correct Giant ion channels allow for the insertion of recording electrodes into the channels.

Properties of the squid’s axons and synapses can be related to its behavior

decreasing sodium outside the cell decreases the size of the action potential.

decreasing sodium outside the cell increases the size of the action potential.

decreasing potassium outside the cell decreases the size of the action potential.

decreasing potassium outside the cell increases the size of the action potential.

manipulating sodium has large effects on both the size of the action potential and the resting membrane potential.

repulsion of positive and negative charges.

diffusion of ions down a concentration gradient.

the greater mobility of small ions.

the selectivity of the membrane to pass positive charges only.

All of the above

The permeability of some ions can be very low.

The permeability of some ions can change over time.

In resting nerve cells, the membrane is quite permeable to potassium.

In resting nerve cells, the membrane is quite permeable to sodium.

All of the above statements are true.

The concentration gradient of the individual ionic species

The permeability of the membrane to the individual ionic species

The sum total of all of the ions on both sides of the membrane

Both a and b

All of the above

makes communication between nerve cells possible.

occurs only in response to external stimuli.

propagates along axons.

determines the cell’s resting potential.

All of the above

Resting membrane

Action

Reaction

Receptor

Synaptic

Electrochemical equilibrium involves the movement of a relatively small number of ions.

Ionic gradients are necessary for the generation of the membrane potential.

The size of the potential is proportional to the size of the ion gradient.

The direction of the ion gradient determines the polarity of the membrane potential.

For a given ion concentration gradient, the resulting potential is independent of the number of charges on the ion.

changing the size of their action potentials.

Correct changing the frequency of their action potentials.

firing at precise moments so as to signal different sized signals.

sending signals of different sizes down different axonal branches.

All of the above

increasing potassium outside the axon depolarized the axon’s potential.

increasing potassium outside the axon hyperpolarized the axon’s potential.

increasing sodium outside the axon depolarized the axon’s potential.

increasing sodium outside the axon hyperpolarized the axon’s potential.

changing external sodium and potassium had identical effects on the resting axon potential.

The current declined when there was decreased driving force on sodium fluxes.

The current disappeared near the Nernst potential for sodium.

The early current was blocked by tetrodotoxin.

The early current was unaffected by tetraethylammonium.

When the late current was blocked, the reversal potential of the inward current shifted to a negative membrane potential.

both currents had the exact same voltage dependence.

both currents increased monotonically with increasingly large voltage steps.

both currents decreased with increasingly large voltage steps.

the early current increased initially, but then it decreased in size as the voltage step was increased.

the late current increased initially, but then it decreased in size as the voltage step was increased.

Myelin sheaths are created by glial cells.

Myelin serves to sharply increase the time constant of the axon.

Multiple layers of closely opposed glial membranes wrap the axon and serve as an electrical insulator.

Myelin is absent at the nodes of Ranvier.

Sodium and potassium channels are clustered at the nodes of Ranvier.

salutatory

scleorid

oligodendroid

ranvierian.

hyperian

Capacitive currents in response to hyperpolarizing voltage steps

Capacitive currents in response to depolarizing voltage steps

A transient inward current as a result of depolarization

A sustained outward current as a result of hyperpolarization

All of the above were seen in squid giant axons.

the sodium current was rapidly activated by depolarization.

the potassium current activates on a comparatively slow time scale of a few ms.

at certain potentials, there can be zero current even with a large conductance.

depolarization leads to a time-dependent inactivation of the sodium current.

depolarization leads to a time-dependent inactivation of the potassium current.

Voltage changes in the cell cannot be seen without voltage clamp.

Ionic conductances can be activated only in cells that have been voltage clamped.

Voltage clamping allows simultaneous control of membrane potential and measurement of permeability changes.

Sodium and potassium currents are activated in non-overlapping voltage regimes.

All of the above

Kenneth Cole.

Alan Hodgkin.

Andrew Huxley.

Bernard Katz.

Alessandro Volta.

The time from threshold to maximum depolarization is essentially instantaneous (i.e., too fast to be measured accurately with current electronics).

A positive feedback loop leads to a regenerative depolarization that would increase continuously if unchecked.

The degree of depolarization is limited in part by the declining driving force on sodium entry.

The degree of depolarization is limited in part by the inactivation time course for the sodium current.

The degree of depolarization is limited in part by the activation time course of the potassium current.

a positive feedback loop between sodium current activation and potassium inactivation.

a positive feedback loop between depolarization and sodium current activation.

a negative feedback loop between sodium current activation and inactivation.

the precise time constant of sodium channel activation (i.e., a threshold would not be observed if this were measurably changed).

pacemaker-like activity that is present in all nerve cells.

A change in permeability of the membrane to sodium

A change in permeability of the membrane to potassium

A transient increase in the sodium current

An initial decrease in the potassium current

A “self-activating” aspect to the rise in the sodium current

MS is characterized by demyelination of axons along with some axon loss.

It was recently proven that all cases of MS are due to persistent infection by a tropical parasite.

Cases of MS vary considerably in terms of severity and progression of the illness.

Symptoms of MS may include weakness, paralysis, double vision, monocular blindness, and abnormal somatic sensations.

Magnetic resonance imaging can help diagnose some cases of MS.

Removal of external sodium

Doubling of external sodium

Removal of external potassium

Doubling of external potassium

Removal of all external cations

at most subthreshold voltages.

only when the cell reaches threshold.

only when the membrane potential exceeds threshold by 5 to 10 millivolts.

intermittently, but usually when the membrane potential exceeds threshold.

only after all of the sodium channels are open.

number of sodium channels along an axon

number of potassium channels along an axon

propagation speed of action potentials

threshold voltage of neurons

ratio of sodium to potassium channels

The spread of a passive signal is limited by the leakage of current out of the axon.

The time course of passive signal spread slows with increasing leakiness of the axon.

The membrane length constant describes how far an action potential can propagate along an axon.

Action potentials can propagate for long distances without decrement.

Action potential propagation requires both current flow along the axon and ion fluxes across the axon membrane.

The voltage dependence of the sodium channels

The voltage dependence of the potassium channels

The presence of a refractory period at a location where an action potential has just passed

Sufficient “leakiness” of the axons, such that backward propagation of action potentials is prevented

The polarized orientation of microtubules within the axon

an action potential is evoked before the current has spread any distance from the point of injection.

the current will spread only in one direction.

the current will spread passively only if it is a depolarizing current.

the current will decay exponentially with increasing distance from the injection site (if no action potential is present).

the current will propagate as an oscillating wave independently of its polarity.

The driving force on the ionic current is the difference between the membrane potential and the ion’s Nernst potential.

The conductance for an ion is inversely proportional to the resistance of the membrane to the passage of that ion.

All permeant ions experience an identical driving force at each time point during the course of an action potential.

The conductance for each ion can be calculated based on the measured ionic currents and the calculated driving force.

The calculations stemming from Ohm’s law can be used to derive a mathematical description of the action potential.

The action potential can be reconstructed based entirely upon the time course and amplitudes of the ionic conductances.

The fast-rising phase can be accounted for by selective sodium entry.

The model mimics the experimentally measured refractory period.

The falling phase can be at least partially accounted for by the activation time course of the potassium current.

The undershoot can be accounted for by the time course of sodium current reactivation.

The movement of a sodium ion produces a larger voltage change than the movement of other ions.

Sodium ion diffusion proceeds so quickly that whenever sodium channels are open, there is a rapid directional flux across the membrane.

The conjunction of the sodium gradient and the negative membrane potential produces a very large driving force on sodium ions.

All of the above

None of the above

abnormally functioning pain receptors in the peripheral nervous system.

enhanced synaptic excitation of second-order pain-sensitive neurons.

abnormal activation of thalamic pain centers.

abnormal activation of neocortical pain centers.

the syndrome by some unknown mechanism

The potassium channels pass only a few ions per second.

The potassium channels show little voltage dependence.

The summing of the individual potassium channels does not reconstruct the macroscopic current.

Once the potassium channels open in response to a voltage step command, they tend to remain open.

All of the above

The IP3 receptor located on the endoplasmic reticulum

The potassium-activated calcium channel

The glutamate receptor

The cAMP- and cGMP-gated ion channels

The acid-sensing ion channels

serve as a plug or inactivation gate.

be the primary voltage sensors

confer ion selectivity to the channel.

enable the aggregation of channel subunits into functional channels.

All of the above

passive transporters.

active transporters.

voltage-gated ion channels.

ligand-gated ion channels.

permeability transition pores.

is much simpler than the sodium–potassium pump because it has only three transmembrane regions.

pumps 15 calcium ions for each molecule of ATP consumed.

uses the same intracellular domain for both nucleotide binding and ion translocation.

pumps calcium in a cyclical process that utilizes energy from ATP.

is unique among transporters in that its pumping action involves no conformational changes.

All transporters are electrogenic.

All transporters transport two or more different ions.

All catalyze the conversion of ATP to ADP.

All are able to move at least one ion against its concentration gradient.

All of the above

there is an obligatory coupling of sodium efflux and potassium influx.

this transporter (or “pump”) is electrogenic.

phosphorylation and dephosphorylation are respectively associated with the sodium and potassium transport steps.

the pump transports two potassium ions for every three sodium ions.

All of the above

were visualized with the advent of the voltage clamp in 1956.

show the same time course as macroscopic ionic currents.

may pass thousands of ions per millisecond.

have a different voltage dependence than the macroscopic ionic current has.

have a different reversal potential than the macroscopic ionic current has.

Dramatic increase of efflux during a brief train of action potentials

Sharp drop in efflux when extracellular potassium was removed

Dependence of efflux upon the presence of ATP

Decrease of efflux when mitochondrial ATP synthesis was inhibited

All of the above were observed.

size of the individual ion channels.

voltage-dependence of the ion channels.

time-dependence of the ion channels.

discovery of differences in ionic selectivity.

sheer number of different ion channels.

The channel pore narrows to fit the size of a non-hydrated potassium ion.

Cations such as cesium are too large to pass through the pore.

Cations such as sodium are too small to be dehydrated at the pore filter.

All of the above

None of the above

With only six different types, potassium channels are the least diverse channel type.

There are at least 10 different sodium channels in humans.

Sodium channels that do not inactivate have been found.

There are least 10 different types of calcium channels.

Calcium channels serve diverse functions such as influencing action potential shape and mediating the release of neurotransmitters.

Cell attached

Intracellular

Whole cell

Inside–out patch

Outside–out patch

complex sequences of voltage commands.

heat and cold.

intracellular cyclic nucleotides.

hyperpolarization.

ultraviolet light.

the sequencing of the channel’s amino acids.

physiological measurements of ion selectivity.

X -ray crystallography

fluorescence imaging of channel subunit dynamics.

All of the above provide similar information on the channel’s three-dimensional structure.

The sodium/calcium exchanger

The sodium/potassium/chloride co-transporter

The sodium/neurotransmitter co-transporter

The sodium/proton exchanger

All of the above transporters have been observed.

Xenopus is the only lower vertebrate whose genome has been sequenced.

The unusually small size of the eggs makes patch-clamping relatively easy.

The oocytes have many endogenous ion channels to which exogenous channels can be compared.

The oocytes have quite thin membranes, which amplifies the ionic currents.

It facilitates physiological characterization of modified ion channel genes.

block sodium channels.

prolong the open state of sodium channels.

alter the voltage-dependence of sodium channels.

block potassium channels.

All of the above

ligand-gated; ion-gated

ionotropic; metabotropic

voltage-gated; voltage-modulated

cationic; anionic

excitatory; inhibitory

are found only in a few species of animals.

are far more numerous than chemical synapses.

have larger pores than voltage-gated ion channels.

are found only where there are large gaps between nerve cells.

are used to pass chemical neurotransmitters.

a; b; c; d; e

b; d; e; c; a

b; e; d; c; a

e; d; b; c; a

a; b; d; e; c

proteolytic cleavage of SNARE proteins.

circumventing the calcium-regulatory step of exocytosis to promote massive exocytosis.

binding to all molecules of synapsin, synaptotagmin, and synaptophysin and thereby preventing their normal functioning.

punching holes in vesicles and thereby causing release of their contents into the cytosol.

blocking calcium channels.

fewer calcium channels in the presynaptic terminals.

a greater rate of spontaneous exocytosis depleting the size of the vesicle pool.

smaller synaptic vesicles.

a change in the sensitivity of the calcium release mechanism.

a loss of all ACh receptors at the neuromuscular junction.

Endosome, coated vesicle, vesicle reserve pool

Vesicle reserve pool, coated vesicle, endosome

Endosome, vesicle reserve pool, coated vesicle

Coated vesicle, vesicle reserve pool, endosome

Coated vesicle, endosome, vesicle reserve pool

Depolarizing currents can be recorded from outside–out patches of postsynaptic membrane.

Individual channels tend to stay open for no more than a few msec.

Acetylcholine can induce openings of ligand-gated ion channels.

The end plate potential is due to the opening of thousands or millions of channels.

The end plate channels show a regenerative opening pattern that propagates an action potential along the length of the muscle fiber.

at miniature end-plates.

by the smallest axons.

in response to weak stimuli.

by the smallest neurotransmitters.

by spontaneous release of neurotransmitter.

Fixed size of MEPPs

Quantized distribution of events occurring at the neuromuscular junction

Visualization of synaptic vesicles using electron microscopy

Correspondence between a vesicle’s acetylcholine content and MEPP size

Visualization of acetylcholine molecules diffusing out of the neck of the membrane-fused vesicle

the ligand-binding properties of the receptor.

whether the permeant ion is positively or negatively charged.

whether the permeant ion’s reversal potential is positive or negative.

whether the permeant ion’s reversal potential is positive or negative to threshold

None of the above

They are much larger than end plate potentials.

EPSPs occurring close together in time can summate and help bring a neuron to threshold.

Multiple EPSPs arriving together at different locations on the dendritic tree can summate and help bring a neuron to threshold.

Their effect in the central nervous system can be nullified by IPSPs.

All of the above are false; none is true.

the depolarization occurs so quickly that the membrane potential goes far positive to 0 mV and produces an overshooting action potential.

there are enough acetylcholine receptors to propagate the action potential along the length of the muscle fiber.

the receptor is also permeable to calcium, which binds to other channels to elicit action potentials.

depolarization of the membrane to 0 mV is sufficient to bring nearby membrane regions, which contain voltage-gated sodium channels, to threshold.

None of the above; acetylcholine does not elicit muscle action potentials

pass small metabolites, including some second messengers.

pass electrical current bidirectionally.

pass electrical current unidirectionally.

amplify small incoming electrical signals into large regenerative potentials.

synchronize the activity of populations of nerve cells.

the acetylcholine receptor channels all close instantly at 0 mV.

an influx of sodium is balanced by an equal efflux of potassium.

the membrane conductance for each permeant ion is 0 at 0 mV.

at 0 mV, the potassium ions lodge in the receptor channel and block the influx of sodium.

the Nernst potentials for both sodium and potassium are 0 mV in muscle fibers.

biophysical differences in the vesicles’ lipids that allow for easier fusion of small vesicles.

a more sensitive calcium-release mechanism on the dense-core vesicles.

a more delocalized calcium signal generated by intense neural stimulation.

the presence of novel fusion proteins on the dense core vesicles that bind neuropeptides.

All of the above

forming a protein coat that maintains the vesicle’s integrity.

binding calcium and then forming a pore into the vesicle.

forming a protein complex that pulls the vesicle membrane against the plasma membrane.

linking calcium channels to exocytotic fusion sites.

pushing vesicles from the reserve pool into the docked pool.

synapsin.

synaptotagmin.

synaptobrevin.

synaptophysin.

snap 25.

It must be present in the presynaptic terminal.

It must be released in response to presynaptic electrical activity.

It must exert an effect on the postsynaptic cell.

All of the above

None of the above

presence of calcium-selective ion channels.

enormous gradient of calcium across the membrane

fact that calcium is a positively charged ion.

fact that calcium is a divalent cation.

All of the above are essential for producing large, rapid concentration changes.

Observation of presynaptic depolarizing currents after blockade of sodium channels

Voltage clamp experiments showing voltage-gated calcium channels in the presynaptic terminal

Induction of transmitter release by injection of calcium into the presynaptic terminal

Blockade of transmitter release by injection of calcium buffer into the presynaptic terminal

All of the above

the neuromuscular junction.

preganglionic synapses of the autonomic (visceral motor) nervous system.

postganglionic synapses of the parasympathetic nervous system.

widely distributed synapses in the central nervous system.

All of the above

can result from very brief (sub-millisecond) increases in glutamate levels.

can be prevented by administration of glutamate receptor antagonists after a stroke has been diagnosed.

has not been correlated with the potency of compounds at glutamatergic receptors.

can occur in some forms of epilepsy and head trauma.

has been linked to a specific intracellular signaling pathway that activates a family of excitotoxicity genes.

the most commonly used neurotransmitter in the brain.

neurotoxic at high concentrations.

a nonessential amino acid.

often synthesized from glial-synthesized glutamine.

all of the above

to treat hypertension.

to treat panic disorders.

as antidepressants.

as antipsychotics.

to treat generalized anxiety.

shortly after their synthesis in presynaptic terminals.

as pre-propeptides.

as propeptides.

more readily and quickly than nonpeptide transmitters.

together with nonpeptide transmitters.

Pyridoxal phosphate

Glutamic acid decarboxylase

GABA transaminase

γ-hydroxybutyrate

Glutamine

two

three

five

seven

nine

1; 2; 3; 4; 5

5; 4; 3; 2; 1

4; 2; 3; 1; 5

2; 3; 4; 1; 5

1; 5; 2; 3; 4

Biogenic amines

Amino acid transmitters

Neuropeptide transmitters

Purinergic transmitters

Gaseous transmitters

neocortex.

the hippocampus.

basal ganglia.

the hypothalamus.

All of the above

Dopamine

Histamine

Norepinephrine

Epinephrine

All of the above are catecholamines.

Dynorphins

Endorphins

Enkephalins

Endocannabinoids

All of the above are opioid peptides.

GABAA

GABAB

GABAC

Glycine

Muscarinc ACh receptor

nicotine

muscarine

conotoxin

α-bungarotoxin

δ-tubocurarine

on GABAA receptors.

as an MAO inhibitor.

by blocking serotonin reuptake.

by blocking dopamine reuptake.

by blocking biogenic amine vesicular transporters.

The presence of multiple glutamate receptor families with different ionic selectivities

Voltage-dependent gating of certain types of glutamate receptor

the passage of large amounts of magnesium and calcium by NMDA receptors

The use of specialized proteins for loading glutamate into vesicles

The use of specialized proteins for removing glutamate from the synaptic cleft

degeneration of lower motoneurons.

degeneration of upper motoneurons.

mutations affecting the synthesis of acetylcholine.

mutations affecting acetylcholine receptors.

an autoimmune attack on acetylcholine receptors.

immature GABA receptors pass more sodium than chloride.

immature GABA-receptive neurons have a more negative firing threshold than mature neurons.

immature GABA-receptive neurons express many Na+/K+/Cl– co-transporters.

immature GABA-receptive neurons express many K+/Cl– co-transporters.

the opening of GABA receptor channels tends to excite immature cortical networks because of the networks’ wiring.

Its presence in many inhibitory neurons

Its ability to block the reuptake of inhibitory transmitters

Its actions as a cofactor at glycine receptors

The consequences of xanthine (e.g., caffeine) blockade of adenosine receptors

The co-localization of adenosine with GABA in GABAergic synaptic vesicles

2; 4; 1; 3

3; 1; 4; 2

2; 1; 3; 4

1; 2; 4; 3

2; 4; 3; 1

Adenylyl cyclase

Guanylyl cyclase

Phospholipase C

All of the above

None of the above

PKA

CaM kinase II

MAP kinase

ras

All of the above contribute to CREB activation

Ion channel-mediated depolarization

G-protein-mediated modulation of ion channels

Phosphorylation of effector molecules by protein kinases

Synthesis of proteins after CREB activation

None of the above; all have similar time courses

were discovered with the invention of electron microscopy in the 1950s.

serve as “electrical compartments” to ensure localized depolarization.

serve as “chemical compartments” to concentrate biochemical mechanisms.

collectively form a set of hard-wired permanent neural connections.

are the sites of all excitatory and inhibitory synaptic transmission in the mammalian CNS.

Voltage-gated calcium channels

The plasma membrane calcium ATPase

The smooth endoplasmic reticulum calcium ATPase

The sodium–calcium exchanger

Mitochondria

They enable localized, transient increases in calcium.

They slow the diffusion of IP3, but do not prevent it from leaving the spine.

They are the sites of excitatory synapses in various parts of the CNS.

They have a bulbous head connected to a dendritic shaft by a narrow neck.

They usually contain just three proteins: NMDA receptors, mGluR receptors, and CaM kinase II.

Protein kinase A

Protein kinase C

Protein kinase G

CaM kinase II

CaM kinase IV

Cellular responses are always short-lived.

Cellular responses are always long-lived.

Signaling is always initiated by membrane-bound receptors.

Signaling is always initiated by intracellular receptors.

None of the above is true; all are false.

Hydrolysis of GTP prior to association of the regulatory and catalytic domains

Reliance on functionally distinct roles of the different domains

Binding of one or more messengers to a regulatory domain

Inhibition of a catalytic domain by a regulatory domain

Activation of a catalytic domain via a protein conformational change

1; 4; 3; 2

4; 1; 3; 2

3; 4; 1; 2

3; 1; 4; 2

1; 3; 4; 2

Calcium

CAMP

cGMP

Inositol trisphosphate

Diacylglycerol

channel-linked receptor.

enzyme-linked receptor.

G-protein-coupled receptor.

nuclear receptor.

gap junction.

Serine and threonine kinases are typically activated by second messengers.

Tyrosine kinases are typically activated by extracellular signals.

Each protein kinase has just one specific target protein that it phosphorylates.

The effects of protein kinases can be balanced by protein phosphatases.

Thousands of protein kinases are expressed in the brain.

Ryanodine receptor

IP3 receptor

cGMP

Phospholipase C

Calmodulin

Endocrine

Exocrine

Paracrine

Synaptic

Ephaptic

Voltage clamp

Fura-2

Calcium green

GFP

Channel rhodopsin

PKA

PKC

CaM kinase II

MAP kinase

All of the above

Alternating activation of climbing fibers and parallel fibers is required to induce LTD.

The firing of parallel fibers activates mGluR receptors and generates IP3.

Climbing fibers generate a large calcium signal in Purkinje cell dendrites.

Both IP3 and calcium are required to activate the IP3 receptors and depress AMPA receptor activity.

The strength of the parallel fiber synapses can be depressed for a long period of time.

regulates cell differentiation.

is a monomeric, or small, G-protein.

is named after the rat sarcoma tumor virus.

All of the above

None of the above

Activation of G-proteins by an activated receptor

Activation of adenylyl cyclase molecules by G-proteins

Creation of cAMP molecules by adenylyl cyclase

Phosphorylation of target proteins by protein kinase A

All of the above are steps in which amplification occurs.

small burns made in cortex by an electrical stimulating electrode.

the ability to induce LTP in the amygdala and other brain regions in live animals.

the ability of daily administration of a weak, low-amplitude train of electrical pulses to gradually evoke larger and larger behavioral responses.

the phenomenon whereby a single, strong electrical pulse can evoke a full-blown seizure.

chaotic patterns of neural activity resembling the flame of a candle.

The ability to behaviorally assay large numbers of animals

Development of an assay that was sensitive to learning and memory deficits

The ability to discriminate learning deficits from sensory and motor deficits

Development of novel apparatus to perform the behavioral assays

All of the above were important.

Activation of G-protein-coupled receptors by serotonin

Phosphorylation of CREB

Activation of adenylyl cyclase

Activation of protein kinase A

Decreased opening of potassium channels during presynaptic action potentials

synergistic actions of calcium and IP3 on internal calcium release channels.

synergistic actions of sodium and IP3 on internal calcium release channels.

activation of AMPA receptors by voltage-gated ion channels.

binding of IP3 to clathrin to activate endocytosis.

calcium-dependent insertion of GABA receptors into the postsynaptic membrane.

The hallmark of both short-term and long-term synaptic plasticity is that they always increase the strength of synaptic connections.

The efficacy of synapses can be adjusted by modulating the amount of neurotransmitter that is released.

Calcium ions play a central role in at least some forms of synaptic plasticity.

Changes in synaptic efficacy can occur over time scales ranging from milliseconds to years.

A variety of molecular mechanisms are involved in the different forms of synaptic plasticity.

phosphodiesterase.

adenylyl cyclase.

adenylyl cyclase activating pathways.

allosteric modulation of GABA receptors.

CREB gene regulation.

History-dependent modification of synaptic efficacy

NMDA receptor activation

Calcium influx

Calcium-dependent activation of protein phosphatases

All of the above are used in both LTD and LTP.

Whether or not LTP occurs depends on the specific temporal pattern of action potentials.

LTP occurs whenever an action potential precedes an EPSP.

LTD occurs whenever an action potential follows an EPSP.

Switching the relative timing of action potential and EPSP by as little as 20 ms can switch the response from LTD to LTP, or vice-versa.

A rhythmic pattern of spike–EPSP–spike–EPSP, at 40 ms intervals, produces maximal LTP.

Area CA1

Area CA3

Area MT

Dentate gyrus

None of the above; all are part of the hippocampus

extra calcium.

lowered calcium.

extra sodium.

reduced sodium.

extra magnesium.

LTP involves an enhancement in synaptic efficacy that can last for hours, days, weeks or even longer.

If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and another nearby synapse (B) on the same dendrite is weakly stimulated at the same time, then the second synapse (B) will also show LTP.

If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and a nearby synapse (B) on the same cell is weakly stimulated a few seconds later, then the second synapse (B) will also show LTP.

The requirement for coincident pre- and post-synaptic activity was predicted by Donald Hebb in 1949.

Hippocampal LTP was first reported by Bliss and Lomo about 1970.

An influx of calcium triggers two or more intracellular processes in the postsynaptic dendritic spine.

Calcium may trigger the release of a retrograde messenger that enhances transmitter release from the presynaptic terminal.

Calcium may activate CaM kinase II in such a way that it switches to a long-term “on” state.

Calcium may activate a signaling cascade that causes the insertion of glutamate receptors into the postsynaptic membrane.

Calcium decreases a resting leak current of sodium so that the postsynaptic cell is closer to threshold and therefore fires more easily.

Inhibition of presynaptic calcium channels

Activation of presynaptic potassium channels

Depletion of docked synaptic vesicles in the presynaptic terminal

Delayed replenishment of vesicles to the reserve pool

Enhancement of presynaptic sodium currents

all glutamate receptors open automatically whenever glutamate is in the synaptic cleft.

the NMDA receptor acts as a molecular coincidence detector

the AMPA receptor allows calcium into the cell only after the NMDA receptor is activated.

both the NMDA and AMPA channels must be open in order for the cell to depolarize.

All of the above are key aspects of LTP induction.

enhancement.

depression

facilitation.

augmentation

potentiation.

voltage-gated ion channels.

ligand-gated ion channels.

synaptic vesicle regulatory proteins.

postsynaptic signaling pathways.

unknown

Mossy fibers

Perforant path

Stratum radiatum

CA1 region

CA3 region

The efficacy of transmission at many synapses depends upon their history of synaptic activity.

The tracking of long-term changes in synaptic efficacy is difficult in mammalian systems because of the complexity of mammalian brains.

The gill withdrawal reflex in Aplysia can be enhanced by pairing a noxious stimulus with a mild touch.

Associative learning in the Aplysia gill withdrawal reflex is relatively independent of the timing or the order in which different stimuli are applied.

Gill withdrawal behavior in Aplysia can be altered for days or weeks by means of repeated pairings of shocks and touches.

AMPA receptor.

NMDA receptor

glycine receptor.

cholinergic GPCR.

noradrenergic GPCR.

have no presynaptic terminal.

have AMPA receptors but no NMDA receptors.

have NMDA receptors but no AMPA receptors.

lack voltage-gated sodium channels.

are continuously inhibited and so cannot be activated.