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160 Cards in this Set

  • Front
  • Back
What is the structure of a neuron? (Left to right)
Dendritic tree - Axon hillock - Axon (long) - synapse
What is the Dendritic tree responsible for? Axon Hillock?
The Dendritic tree is responsible for synaptic inputs

The Axon hillock is responsible for initiating the action potential
What is the Axon (long) responsible for? The Synapse?
Axons are responsible for fast electrical transmission

Synapses are used for chemical transmission between neurons
How does the Axon conduct electricity so fast? What is the name of the fluid in the axon?
the axoplasm (fluid in the axon) conducts electricity and the axon membrane acts as an insulator like the plastic coating around a wire
What happens when axon electrical signals have to travel farther?
The signal becomes smaller with less electrical signaling than in the shorter distances
What are some reasons that there is electrical decay when electrical signals are transmitted through the axon?
The axoplasm is not a perfect conductor (it has electrical resistance)

The axon membrane is not a perfect insulator

The axon membrane acts like an electrical capacitor and stores some of the electricity charge flowing through the axoplasm
What is the axoplasm? What is one small disadvantage of its conduction?
A solution of salts that acts as the fluid in the axons to conduct electricity, but it is not a perfect conductor
How thin are axons?
How long are they? How far do electrical signals have to go to begin to decay?
Axons are a few micrometers thick and more than 1 meter long

electrical signals decay within a few mm
What is passive conduction usually limited to in signal along axons? How do axons get around this problem?
a few mm

Axons get around this problem by active transmission, where a regenerative signal called an action potential is fired and boosted as it travels along a nerve
How are concentration gradients established in nerve cells? (what is the specific protein)
ion pumps
How are Ion channels different from ion pumps?
Ion channels allow for selective permeability of the membrane to certain ions, ion pumps establish concentration gradients in the cell
What is a diffusion potential? What is a simple example of a diffusion potential?
A voltage generated by passive diffusion of ions down a concentration gradient

KCl put in solution and allowed to dissociate with a membrane in the middle that only allows for K+ permeability, makes it so there is a potential difference, which is the diffusion potential
What is the relation between concentration difference and the resulting diffusion potential (at equilibrium with K+ and Cl-)?
At equilibrium work in moving K+ ion up the concentration gradient must equal work in moving against the electrical gradient
What is the Nernst equation?
E=58mV*log10([K+ right]/[K+left])

Where E is the equilibrium potential
If you plug in 10 M for K+right and 100mM for K+left, what do you get from the Nernst equation?

What about 1M for K+right and 100mM for K+left?
116 mV

58mV
How many K+ ions need to move to establish the equilibrium potential?
only enough to charge the membrane capacitance
What is special about squid axons? how much bigger are they than mamallian axons?
They are fucking huge, 100 to 1000 times larger than mammalian axons
What does the actual potential in a cell depend on?
the relative permeability of the membrane to each ion that comes in and out
During an action potential, what is there a larger permeability of in the membrane? At rest which has a larger permeability?
During an action potential, Sodium (Na+) ions permeate the membrane more freely

During resting potential, K+ permeability is much higher than other ions
What does increased permeability of ?Na+ and K+ ions during action and resting potentials result in?
the action potential will be closer to ENa and the resting potential will be closer to EK+
What is the Goldman equation used for?
measuring the voltage across a membrane permeable to multiple ions
How would you measure the voltage of a membrane permeable to multiple ions?
you would use the Goldman equation
What is the goldman equation? Where are positive ions going out located in it? What is P in these equations?
V=58mV log (Pk[K]out+PNa[Na]out+Pcl[Cl]in)/(Pk[K]in+PNa[Na]in+Pcl[Cl]out)

Positive ions going out are in the numerator

P is permeability
What is the experimental evidence that resting potential is set by K+ concentration gradient?
There is a shallow slope for K+ out as permeability to other ions becomes more significant

slope = 58 mV, which indicates a 10 fold change in K+ concentration gradient
What is the slope of Na+ ions at resting potential?
close to 0
What is the slope of Na+ out (on x axis) and membrane potential (on y axis) at the peak of action potential?
58 mV per tenfold change in Na+ gradient
What are the relative slopes of membrane action potential versus Na+ and K+ out at action potential and resting potential?
58 mV/10 fold change in Na+ gradient
What is the action potential?
A regenerative depolarization that propagates actively along a nerve or muscle cell
What does the action potential look like graphically (and some of the parts of it labeled?)
there is first resting potential, then stimulus artefact, then conduction delay and then the rising phase, a peak with an overshoot, then the falling phase, and then the after potential and the undershoot
What triggers an action potential? What does hyperpolarizaton evoke?
A threshold level of depolarization is needed to trigger an action potential

hyperpolarization evokes only passive responses
Why are only passive responses seen when hyperpolarizing an axon rather than an action potential, what properties of the axon does this?
the passive responses are due to membrane properties like resistance and capacitance
What is special about the amount of depolarization and the size of the action potential?
Action potentials are all-or-none events - Once a stimulus exceeds threshold the size of action potential is independent of stimulus strength
What is special about action potential propagation? How fast is it?
Action potentials stay the same size as they travel along an axon

action potentials are fast, but a million times slower than an electrical signal through a wire
What is the refractory period? Why is this important?
It is the period after an action potential has been fired, where there is a short time in which the axon cannot be stimulated to give another action potential

This is important because it stops action potentials going backwards and it sets a limit to the maximum number of action potentials a nerve can transmit
What is a more descriptive way of describing the action potential?
a brief time when the membrane potential is flipped positive rather than negative inside due to a higher permeability to Na+ ions that rush into the cell and depolarize it.
What happens during the rising phase of an action potential? (Na+ channels)
Depolarization opens voltage-sensitive Na+ channels

Na+ enters the cell causing depolarization
What happens during the falling phase of action potentials?
Na+ chanels inactivate = no more depolarizing

Extra K+ channels slowly open in response to depolarization

Efflux of K+ ions from cell hyperpolarizes it back toward the K+ equilibrium potential
What are the equilibrium potentials of K and Na?
Ek = -80 mV and ENa=60 mV
At rest what are the ion channels like?
small resting permeability to K+, virtually no permeability to Na+
During the rising phase what are the ion channels like? What is the Equilibrium voltage like?
Na+ channels open in response to depolarization, Na+ influx causes more depolarization, so more channels open, so more depolarization etc.

The Na+ permeability is much greater than K+ permeability and so the potential at the peak of the action potential is close to ENa
In the falling phase what are the ion channels like?
Na+ channels inactivate in about 1ms

K+ channels are voltage dependent - they open with depolarization, but much more slowly

K+ permeability is much greater than Na+ permeability so the potential quickly returns toward Ek, which is -80 mV
How much Na+ enters an axon during an action potential? How much does intracellular Na+ rise during an action potential?
very little, only enough to charge the membrane capacitance from -80 mV to +60 mV

Intracellular [Na+] rises less than 1% during a single action potential
If an Na+ pump is poisoned, how many action potentials can an axon transmit?
still greater than 1000 action potentials can be transmitted by an axon with a poisoned Na+ pump
What is the voltage clamp and who was it used by?
Technique that allows voltage across axon membrane to be held at any level, and then you measure the current flow across the membrane

used by Hodgkin - Huxley
What happens when voltage activated currents in response to a voltage clamp depolarizing step?
first there is a depolarizing, inward current that slows and becomes smaller and then inverts direction, and then a sustained outward current is achieved
When you dissect the components of what happens when you depolarize a nerve?
A normal solution that has inward current and then it inverts to outward current, and then a low [Na+] solution that starts and then rises steadily from the x axis
What is TTX and what does it do?
TTX is tetrodotoxin and it selectively blocks Na+ current
What is current proportional to?
The number of channels open times the voltage making current flow
What is the conductance equation?
g = I/(V-Veq)

where g is the conductance, I is current, and V is membrane potential and Veq is equilibrium potential for the particular ion
what is conductance equal to?
conductance is 1/resistance
What is the relationship between Voltage and inward or outer current with Na+?
when there is inward current there is depolarization, and the inward current will increase during an action potential because more channels are open

increasing outer current means reduced voltage for Na+ influx
What happens in the resting and rising phase to Na+ conductance? falling phase?
In the resting phase almost no Na+ channels are open so conductance is 0,

It goes up because of all of the channels that are open, there is less resistance, and conductance is 1/resistance

In the falling phase, Na+ conductance slowly decreases because Na+ channels are beginning to close
What happens to K+ conductance during the rising phase, peak, and falling phase of action potentials?
Slow increase in conductance during the rising phase because a few K+ channels are open
What do the membrane conductances for Na and K look like?
They are both just humps, but the Na hump is sharp and quick, while the K hump is broader and takes longer to come up as well as decrease
Why do gNa and gK fall?
GNa falls because of inactivation of channels, and gK falls (with some delay) because the membrane re-polarizes
What does an action potential propagate? what is an active zone?
the axon behaves like a passive electric cable to transmit depolarization

an active zone is a zone around the action potential on the axon at a specific point in time while it is propagating
What does the local current flow do when an action potential is propagating down an axon?
depolarizes the axon on either side of the action potential, thus triggering action potential there
Why does an action potential travel only one way?
action potential only travels in one way because the axon behind the action optential is refractory (Na+ channels are still inactivated), so only the region ahead of the action potential can be stimulated
What does orthodromic mean? What does it have to do with?
Orthodromic means that something only goes in one direction

This is used to describe action potentials going only one way on the axon
How can you get action potentials going backwards? What is this called when something goes backwards?
You can artificially stimulate to get backward action potentials, this is called antidromic
What happens in the propagation of an action potential (looking just at channels opening in response to an initial stimulus)?
Na+ channels open in response to stimulus

Depolarizing current flows down axon, and the local depolarization causes neighboring Na+ channels to open

upstream Na+ channels inactivate while K+ channels still open
this proces repeats
What determines the speed of propagation of an action potential?
How fast the next region of the axon can be depolarized to the threshold for it to generate an action potential
When is the speed of propagation of an action potential faster in terms of low or high resistance and capacitance of the next region of the membrane?
propagation is faster when the resistance and capacitance of the axoplasm is smaller
What is one way to make an axon transmit action potentials faster? Why is this the case?
Make it fatter by increasing the radius,
axoplasmic resistance varies with cross-sectional area of axon
What do resistance and capacitance vary with respect to r?
Resistance will vary as 1/r^2 and Capacitance will vary as r

R --> 1/r^2

C--> r
What is the net effect as r increases on R and C and conduction velocity?
both resistance and capacitance decrease so that conduction velocity increases
What is another way to help make action potentials propagate faster? Why?
Wrap a myelin sheath around the axon

the myelin sheath increases effective thickness of axon membrane many-fold

thus capacitance is greatly reduced, speeding action potential
What is saltatory conduction?
when an axon is completely wrapped in myelin except for the Na+ channels and the action potential jumps rapidly from the nodes of the open channels.
What are Ion channels?
Protein molecules in lipid membrane forming aqueous pore through which ions can permeate
What is the total current given by?
the number of channels open times the current through each channel
What is the current through single channels usually?
a few pA (10^-12)
At a single node, how many Na+ channels are there?
about 1 million Na+ channels
What is one way to study ion channels? How does it work (patch)
Functional studies - patch clamp

glass pipettes are pressed against cell to form a seal with the membrane and the current flowing through the channel in the membrane patch under the pipette is measured by an amplifier
How do single channel currents work? How long are the durations of each opening and closing?
the single channel currents switch between open and closed states, producing rectangular pulses of current

The durations of the opening and closing are random, but the current is the same for each opening
What do we know about the molecular structure of ion channels?
genes for many ion channels have been cloned and sequenced. We know the primary structure of the channel protein and can predict secondary structure (protein folding)
How are ion channels formed? What are the ion channel proteins embedded in?
from several building blocks, like protein subunits or homologous repeats within a single giant protein like C9 to form an aqueous pore.

ion channel proteins are embedded in the lipid bilayer
What is channel gating controlled by?
membrane potential and the binding of agonist molecules to the receptor site on channel protein (like acetylcholine receptor at muscle endplate)
What are Gating currents?
special regions in each domain of the Na+ channel that have strong electrical charge. They act as voltage sensors (that can detect membrane potential and whether it's time for an action potential) by moving across the membrane in response to electric fields.
What does the sodium pump do? How are concentration gradients with, say, K+ and Na+ generated?
exchanges K+ for Na+, with K+ coming into the cell and Na+ going out. This establishing of concentration gradients is done by Na+ or K+ ATPase which uses metabolic energy provided by ATP.
How much of the energy requirement in a resting neuron does the Na+ channel take? After electrical activity?
In a resting neuron, the Na+ channel accounts for 1/3 of total energy requirement, and after electrical activity the pump accounts for 2/3 of the energy requirement of the neuron
How many K+ ions to Na+ ions are pumped by a sodium ion pump? What does this cause for the cell? How big is this effect?
The Na+ pump is electrogenic, where 3 Na+ ions go out for every 2 K+ ions that go in.

This causes the cell to hyperpolarize and become more negatively charged because more Na+ is moving out than K+ moving in.

this hyperpolarization is not that big and is slight
Why does the resting potential arise in a neuron?
the resting potential arises because of the concentration gradient established by the pump, not because the pump directly generates a voltage
What is synaptic transmission?
transmission of signals between two nerve cells or nerve to muscle cell. Can be electrical or chemical
How does electrical synaptic transmission work? Does electrical transmission allow for synaptic inhibition?
gap junctions form aqueous pores linking cells. Direct electrical current flows from one cell to the other

No, electrical transmission doesn't allow for synaptic inhibition
How does chemical synaptic transmission work?
vesicles hold neurotransmitters and cross the synapse from the presynaptic terminal to the post synaptic cell, which produces an electrical response
What are some characteristics of chemical transmission?
pre and post-synaptic terminals are differentially specialized

transmission goes only one way

action of neurotransmitter can be excitatory or inhibitory, depending on the nature of the transmitter and the receptor
What are the stages in chemical synaptic transmission?
1. Action potential in presynaptic nerve
2. Ca2+ ions flow into nerve terminal
3. Ca2+ ions trigger release of neurotransmitter
4. Transmitter diffuses across synaptic cleft
5. Transmitter acts on postynaptic receptors to allow current flow through ion channels
6. transmitter is destroyed or removed
Who discovered the quantal nature of transmitter release? When? How?
Katz, early 1950s

He used a nerve ending and an end-plate (synapse) to see when an action potential would be triggered by end-plate potentials
Describe what happens to end plate potentials when a nerve is stimulated
Stimulating nerves evokes large depolarization at muscle end-plates, which normally triggers action potentials that contract the muscle. e.p.p. (end plate potential) is due to a massive release of transmitters (acetylcholine:ACh) from the nerve terminal

there is also a tiny spontaneous depolarization without stimulating the nerve that are due to spontaneous releases of Acetylcholine from the nerve
What are m.e.p.p.s.?
miniature end-plate potentials
How many quanta does it take to evoke an e.p.p.?
100 quanta of transmitter
In a normal solution, how much bigger is an e.p.p. from an m.e.p.p.?
100x bigger
If the concentration of Ca2+ is lowered, what happens to the size of e.p.p.?
the size of e.p.p. gets smaller and they occur as multiples of the sizes of m.e.p.p.s.

e.p.p.s MUST BE EVOKED by quanta
What is special about e.p.p.s?
they are quantized, the transmitter is released in packets corresponding to the amount of transmitter in an m.e.p.p.
What does Ca2+ entering the nerve terminal do?
increases the probability of release of quanta - The more Ca2+, the greater the average number of quanta released
What are vesicles? What do they do?
membrane sacks containing a few thousand molecules of transmitters that move towards the synapse and release their transmitters
What do Vesicles do in detail when they are going to be released?
vesicle bind to cell membrane through proteins and form a fusion pore from which the transmitter can be released

Ca2+ causes the proteins in the vesicle and cell membrane to form the fusion pore.

the pore enlarges and bursts open, allowing the vesicle to fuse with the cell membrane
What does transmitter release vary with in the nerve terminals? What does this mean?
Ca2+ concentration, varies to the fourth power with the concentration of Ca2+ ions,

this means that Ca2+ must be regulated tightly in the blood
How can you mimic synaptic transmission?
you inject Ca2+ into a nerve terminal, it will evoke transmitter release
What triggers transmitter release in cells? Electrical current carried by Ca2+ ions or the concentration of Ca2+ ions?
intracellular Ca2+ concentration
How many different neurotransmitters are there?
more than 100 compouds, each have their own receptors that produce different responses
What are the three criteria to define something as a neurotransmitter?
they must be present in presynaptic terminal

They must be released by presynaptic depolarization

They must have specific receptors on the post-synaptic cell
How are neurotransmitter different from hormones? What is across between them that blurs the distinction?
neurotransmitters act on single, or a few postsynaptic cells, while hormones are released into the bloodstream and affect distant organs

A cross between neurotransmitters and hormones is NO because it diffuses readily to affect many cells
What are the different categories of neurotransmitters?
Large molecule neurotransmitters

Small molecule neurotransmitters
What is an example of a large molecule neurotransmitter and small molecule neurotransmitters? (what are the TYPES)
Large molecule neurotransmitters - Neuropeptides

small molecule neurotransmitters - Acetylcholine
Amino acids

Catecholamines

Indolamines
What are some examples (specific chemicals) of small molecule neurotransmitters?
dopamine

norepinephrine

epinephrine
What happens in the synthesis, packaging, secretion, and removal of small molecule and large molecule transmitters in the neuron?
small-molecule transmitters are synthesized and then slowly transported through axons where they are then packaged and then transported to the terminal

Large molecule neurotransmitters are synthesized and then transported with enzymes and pre-peptide precursors along the axon, and then the enzymes modify pre-peptides
How long does neurotransmitter exo and endocytosis take? Endocytosis alone?
1 minute

endocytosis alone takes 10-20 seconds
What are the stages of vesicular exo and endocytosis?
Budding from the endosome, docking near the side of the membrane, then priming for release, then fusion, and budding again and then release back to the endosome

so

Endosome-budding-docking-priming-fusion-budding--->endosome
What makes Acetylcholind into Acetate and Choline?
Actylcholinesterase
What happens in the termination of transmitter action in the case of ACh?? In a general case?
Acetylcholinesterase breaks down ACh which terminates transmitter action

In general cases, many other transmitters are not broken down in the synaptic cleft. Termination is usually by active transport back into the nerve terminal or glia
What happens to peptides after serving as neurotransmitters?
they diffuse away and terminate
Many drugs that treat psychiatric disorders work by what mechanism? (involved neurotransmitters)

What is an example of these?
the drugs often work by acting on transporters or enzymes that snthesize or degrade transmitters in the nerve terminal.

Prozac blocks reuptake of serotonin
What are end-plate channels? What is their structure like?
Neurotransmitter receptors, it is a protain with 5 subunits

End-plate channels have a binding site for ACh, and a receptor/channel protein with a gate that is opened by ACh
to what ions are end-plate channels permeable to?
Na+ and K+
What does increasing ACh do to end-plate channel openings? What does it not affect?

What does this mean for a graphical representation of open/closed channels?
increases the frequency of channel opening,

does not affect the duration of opening or size of the current through the channel

This means that when ACh is bound, the graphical representation of the channel will have many more peaks and low points
What happens to the overall current at the endplate when there is more ACh? Why?
the overall current increases, because ACh binding makes it so that there are more channels open at any given time
How many AChs must bind to open the end-plate channel? where do they bind?
2 ACh's must bind to allow for opening of end-plate channels
How does the end-plate channel opening vary with respect to ACh concentration?
channel opening increases as the square of [ACh]
If you double [ACh] near end-plate channels, what happens to the probability that a single site will bind ACh? What about the probability that both sites bind ACh?
if you double [ACh], the probability that a single site will bind ACh doubles

the probability that both sites bind ACh quadruples
What happens to choline after it is created by the hydrolysis of Acetylcholine by acetylcholinesterase?
It is recycled by the nerve to make more ACh
What are end plate potentials and miniature end plate potentials in my own words?
e.p.p. s are the depolarization that happens when neurotransmitters go across to the postsynaptic terminals

miniature end plate potentials are when a small amount of acetylcholine gets into the postsynaptic terminals and causes a very slight, VERY slight depolarization
Because the end-plate channels let through Na+ and K+ ions, what do we know about the equilibrium potential?
the equilibrium potential is midway between the equilibrium potentials for Na+ and K+
If the maximum amount of ACh is released onto the end-plate channels, what is the maximum that it can depolarize a muscle fiber?

What does this mean in terms of triggering an action potential?
the end-plate potential cannot depolarize a muscle fiber beyond -10 mV

-10 is more than enough to trigger action potentials, as they are triggered at around -55 mV
What is the threshold of depolarization for triggering an action potential?
-55 mV
What is the resting potential for an endplate? What does the current through end-plates tend to depolarize to?
resting potential is around -90mV in the muscle fiber

currents in the end-plates tend to depolarize to around -10 mV
What does the potential of an end-plate depend on?
the relative conductance of end-plate (how many channels are open)
What is conductance basically??
how many channels are open,

the ease with which electricity can flow
What is the equation for final voltage at muscle E?
E= (gACh x EACh + grest x Erest)/(gAch+grest)
What are the 2 different kinds of receptors when talking about end-plate channels?
ionotropic receptors and metabotropic
What are characteristics of ionotropic receptors?
in ionotropic receptors the receptor site and ion channel are part of the same molecule

ionotropic receptors mediate fast synaptic responses, direct through-put of signals in the nervous system
What are characteristics of metabotropic receptors?
in Metabotropic Receptors the receptor and channel are different proteins, physically separated in the cell membrane. The link between them is a diffusible intracellular second messenger
What are second messengers? What are examples of secondary messengers?
in Metabotropic receptors since the receptor and channel are different proteins, they need a second messenger to send a signal to regulate the opening of the ion channels

Examples of second messengers are cAMP, cGMP, inosital trisphosphate, and diacylglycerol
How do second messenger work? (after a neurotransmitter binds...)
After the binding of a neurotransmitter, GTP binds to a G protein at the bottom of the receptor, and then the G protein dissociates into two pieces (G alpha and G beta gamma)

One of these may control the opening of the ion channel or a G protein subunit can cause an enzyme to make another second messenger, which then controls the ion channel
Are second messenger mediated responses slow or fast?
slow, prolonged, not as fast as ionotropic receptors
What is excitation and inhibition of the postsynaptic terminal usually described as?
excitation is - current flow through ion channels that tends to depolarize the cell toward the threshold for triggering action potential

Inhibition is when current flows through channels that tends to stop action potentials from firing (but does not necessarily hyperpolarize the cell)
What determines whether a given synapse is excitatory or inhibitory?
what particular ions are going through the channels i.e. is the channel hyperpolarizing or depolarizing
What is an example of a an excitatory and inhibitory neurotransmitter?
glutamate is almost always excitatory and GABA is inhibitory
What is temporal summation?
when one excitatory post-synaptic potential is not enough to depolarize a postsynaptic cell to the threshold for an action potential the cell uses several action potentials in quick succession to sum up to the action potential threshold

in other words, you can stimulate the cell more than once to add up to the threshold
What is spatial summation? How is this different from temporal?
When action potentials in several presynaptic nerves give excitatory postsynaptic potential that sum up to reach the threshold

This is different from temporal summation because there is more than one presynaptic terminal/action potential involved whereas in temporal there is only one that is stimulated multiple times
What are inhibitory conductance changes?
When inhibitory receptors are stimulated, transmitters like GABA opens channels permeable to Cl- ions so it makes the cell move its potential towards the equilibrium potential of Cl- ions, which is -80
What is spatial summation? How is this different from temporal?
When action potentials in several presynaptic nerves give excitatory postsynaptic potential that sum up to reach the threshold

This is different from temporal summation because there is more than one presynaptic terminal/action potential involved whereas in temporal there is only one that is stimulated multiple times
What is the equilibrium potential of Cl- ions in neurons? What does this mean when GABA opens Cl- channels?
-80

This means that when GABA opens the Cl channels the cell will move towards -80 whether it is above or below
What are inhibitory conductance changes?
When inhibitory receptors are stimulated, transmitters like GABA opens channels permeable to Cl- ions so it makes the cell move its potential towards the equilibrium potential of Cl- ions, which is -80
GABA can cause depolarization, how is this possible when it is an inhibitory neurotransmitter?
the depolarization caused by GABA only makes the cell go up to -80, which is well below the threshold for action potential
What does the Cl- current by GABA activated channels do?
tends to hold the cell at -80 mV, which opposes depolarization from excitatory synapses
What is the equilibrium potential of Cl- ions in neurons? What does this mean when GABA opens Cl- channels?
-80

This means that when GABA opens the Cl channels the cell will move towards -80 whether it is above or below
GABA can cause depolarization, how is this possible when it is an inhibitory neurotransmitter?
the depolarization caused by GABA only makes the cell go up to -80, which is well below the threshold for action potential
If a postsynaptic terminal has both excitatory and inhibitory inputs, what does the potential depend on?
the potential would depend on the relative sizes of the excitatory and inhibitory conductance changes
What does the Cl- current by GABA activated channels do?
tends to hold the cell at -80 mV, which opposes depolarization from excitatory synapses
If a postsynaptic terminal has both excitatory and inhibitory inputs, what does the potential depend on?
the potential would depend on the relative sizes of the excitatory and inhibitory conductance changes
What is a pore loop?
the part of the channel protein (ion channel) that determines its ionic specificity, it is a region of hydrophyllic amino acids in each subunit that come together in a complete channel molecule to form an aqueous pore
What is a quantum of transmitter?
the amount of neurotransmitter released by a single presynaptic vesicle
Why is spatial summation of an excitatory postsynaptic potential in a neuron possible?
the neuron membrane acts like a passive electrical cable
Why is the conduction velocity of a myelin-sheathed axon faster than an unmyelinated axon?
Myelin increases the separation between the axoplasm and the extracellular fluid
What is a key difference in small molecule and peptide neurotransmitters?
Peptide neurotransmitters are synthesized in the cell body, but smll molecule neurotransmitters may be synthesized by enzymes at the presynaptic terminal
What are the kinetics of an endplate potential largely determined by?
the capacitance of the muscle membrane
Where are sodium channels located in a myelinated axon?
the nodes of ranvier
In glutamate reuptake, where is it taken from?
the synaptic cleft
What does myelin do to the thickness of the axon membrane? What does this do to capacitance?
Myelin increases the effective thickness of the axon membrane, which decreases membrane capacitance