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72 Cards in this Set

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  • Back
How does axon diameter effect conduction spped?
increasing the diameter increases speed because it decreases internal resistance and allows for more ion channels
What effect does more membrane from a wider axon have on capacitance?
more mebrane, capacitance increases, more area to separate charge
How does axon diameter effect conduction spped?
increasing the diameter increases speed because it decreases internal resistance and allows for more ion channels
What effect does more membrane from a wider axon have on capacitance?
more mebrane, capacitance increases, more area to separate charge
How does a longer length constant effect conduction velocity
a longer length constant means a fater conduction velocity because the membrane resistance is high and the longitudianl resistance is low
In a current clamp experiment, you control.... and measure ....
In a current clamp experiment, you control current and measure voltage, current is injected and changes in Vm are monitored
In a voltage clamp experiment you control...and measure....
In a voltage clamp experiment you control voltage and measure current
How is voltage controled in a voltage clamp experiment
in equal and oppositve current is injected to keep the membrane voltage constant
How can Ohm's law V=IR be rewritten to use during a voltage clamp experimen
Ix= gx (eclamp- Ex)
Ix is the current for a particual ion, gx is the conductance (the inverse of resistance) and (eclamp- Ex) is the net voltage of the clamp minus the equilibrium voltage for the particular ion (can be figured out with nernst equation)
describe an IV plot
An IV plt gives you a profile of the voltage dependent behavior of an ion channel, you can figure out the equilibrium voltage potential for a particular ion by finding where current= 0 on the graph
what is the purpose of patch clamping
you control the voltage and measure the current through a single ion channel
how can you use current clamping to figure out the theshold potential?
Inject increasing amounts of current/ ions and watch for the membrane voltage to reach threshold and generate an action potential
in a current clamp experiment, injecting a "negative current" will .... the membrane and a positive current will ... the membrane (think in terms of polarization)
injecting a negative current will hyperpolarise the membrane, injecting a positive current will depolarize the membrane
In a voltage clamp experiment, how would we expect the current to change if a hyperpolarizing voltage was maintained
the current would not change because the hyperpolarizng voltage would not lead to an action potential
How would we expect the current to change if a depolarizing voltage was maintained
the current would increase. flow out of the cell because the cell would become inside positive
why will conduction velocity be slower if the time constant is longer?
the time it takes for the next region of membrane to charge will take longer because it takes longer to charge the capacitance even though it stays charged longer
what type of junction can be found at electrical synapses
gap junctions
What is an epsp
An post synaptic potential that brings the membrane potential closer to threshold (depolarizes)
what is an ipsp
a post synaptic potential that brings the membrane farther away from threshold (hyperpolerizes)
what is temporal summation and what property of the mebrane allow for it
temporal summation is the addition of post synaptic potentials over short time intervals, the time constant allows for temporal summation to occur
what is spatial summation and how what property of the membrane allows it to occur
spatail sumamtion is the sum of posp synaptic poteintails from different presynaptic cells, the length constant allows this to occur
what is curare
a toxin that blocks Ach neurotrasmitter receptors and causes a failure of muscle action potential by preventing / lowering the generation of an epp, by stopping the action potential in the muscle cell, researches could study the epp by itself, they determined that the epp spreads electrotronically and does not regenerate like the action potential does the AP in the motor neuron remains uneffected
what are endplate potentials
depolarizations that occur in response to action potentials from the motor neuron before the muscle action potential is generated, they travel electrotronically and do not regenerate like action potentials do
how can the post synaptic current be measured?
you can voltage clamp the postsynaptic membrane
why does a postsynaptic potential last longer than a postsynaptic current
The time course of the potential depends on both the duration of the current and the time constant. The current will end as soon as the transmitter leaves the receptor because the channels close but because of the delay caused by the time constant, the membrane voltage remains even after the current has ended
what controls the direction and intensity of the postsynaptic current
the size of the conductance through the open channels and the electrochemical driving force and charge on the permeant ions
Describe the depolarizing postsynaptic current at the neuromuscular junction
it consists of an influx of Na+ that is partly canceled by a simultaneous flow of K+ ions, this occurs because the postsynaptic ligand gated channels are peremable to both ions
What determines wheter or not synapse will be inhibitory or exitory
the properties of the channels that are open by the transmitter and the identies of the ions that flow through them, it has nothing to do with the transmitter itself
what determines the amplitude and sign of the postsynpatic potential?
the transmembrane voltage prior to the postsynaptic potential and the species of ion(s) carrying the current
what happens to the driving force on a particular ion as Vm approaches Ex
the driving force decreates, when Vm=Ex there is no current flow across the membrane even though the channels are open, if the voltage is clamped on the other side of Em, the current will flow in the opposite direction and the sign of the postsynaptic potential will be reversed
Define reversal potential
when the postsynaptic channels open, the postsynaptic current causes Vm to shift towards Erev which is the membrane potential at which no current flows through the channels
how can the reversal potential be calculated if a single ionic species carries the postsynaptic current
the Nernst equation
How can the reversal potential be calculated if multiple ionic species carry the postsynaptic current
the goldmann equation
what is the relationship between Ik and Ina (the current carried by postassium and the current carrier by sodium) at the reversal potential
they are equal and opposite becase the reversal potential is defined as the point where no net curret is flowing
Given that the Ach activated channels are approximately equally permeableto Na and K, what do the magnitudes of the currents depend on?
the driving force of each ion which is measure as the differnce between the membrane voltage and the equilibrium potential for that ion (Vm-Ex)
what equation represents the driving force on an ion/ how is it defined
Vm-Ex, the difference between the membrane voltage and the equilibrium potential of the particular ion
If the membrane potential of a postsynaptic cell is equal Ena, what happens to the curret?
the current will flow out because the driving force for potassium to leave the cell is high
if the membrane potential of a postsynaptic cell is less than Ena but greater than Erev, what will happen to the current?
The current will flow out but not with the same magnitude as when Vm=Ena
what happens to the current when Vm= Erev
the current is 0, there is not net flow of ions
what happens to the current in a postsynaptic cell if Vm is less than Erev but more than Ek
the current flows in because the driving force for sodium is high, it does not flow in as fast as it would if Vm= Ek
what happens to the current when Vm= Ek
the current flows into the cell because the driving force on sodium is large
what determines the maximum change in Vm after the postsynpatic channels are opend?
Erev, once Vm approaches Erev, the net driving force on the permeant ions drops to 0 and Vm cannot change anymore
If the Erev of a postsynaptic current is more positive than the threshold of the postsynaptic cell, what type of synapse is it?
ecitatory, since Erev is more positive than the threshol, the current flowing in will be able to depolarize the membrane past the threshold before it reaches the point where it can't flow anymore
if Erev is more negative than the theshold of the postsynaptic cell, what type of synapse is it?
if Erev is more negative than the threshold, the synapse is inhibitory because the current reaches 0 before it can depolarize the membrane enough to reach threshold
Inhibitory postsynaptic currents are usually carried through channels permeable to ... and ... because...?
inhibitory currents are usually carried through channels permeable to K+ and Cl- because Erev for K+ or Cl- is closer to Vrest which is more negative than the threshold. By reaching Erev before the theshold, current reaches 0 before the threshold can be met
If Erev is more positive than Vrest, is the the synapse necesarily excitatory?
No. Even though Erev is more positive than Vrest, it still may be more negative than the threshold. The current will still be depolarizng but not depolarizing enough to reach threshold
describe presynpatic inhibition
an inhibitory transmitter is released from a terminal that ends on the presynaptic termianl of an excitatory axon, it reduces the amount of transmitter released from the ecitatory axon which in turn reduces excitation in the postsynaptic cell
Some transmitters modify calcium channels in the presynaptic membrane and make them less resonsive to depolarization. How would this effect the release of transmitter molecules
this is an example of presynaptic inhibition, transmitter release is dependent on calcium entry into the terminal so reducing calcium entry reduces transmitter release
Compare the effects of pre and post synaptic inhibiton
postsynaptic inhibition globally reduces the exitability of the postsynaptic cell making it less able to respond to any exitatory input, presynaptic inhibitoin acts only on 1 specific input so the cell can still respon normally to all other inputs
describe presynaptic release of neurotransmitters
released in packets called quanta in a manner similar to exocytosis
how do we know that neutransmitters are release in quanta
there is minimal end plate potential that is caused by the release of a discrete number of NT molecules, the magnitude of the potential increases in discrete units as the number of quanta increases
The release of a NT vesicle from the readily releasable pool depends heavily on...
the intracellular concentration of calcium
which toxin blocks sodium channels
tetrodotoxin TTX
which toxin blocks potassium channels
TEA tetraethylammonium
what is the relationship between transmitter release and depolarization
more depolarization leads to more transmitter release
Does transmitter release depend on the prescence of an action potential
no, reference Katz's experiment when TTX and TEA were used to block channels and prevent an AP,and the Vm of the presynaptic cell was controlled experimentally. They showed that the amount of transmitter release varied directly with the amount of depolarization that occured
does NT release depend on the chemical identity of the ions causing the depolarization
no, release will occur in proportion to depolarization reguarless of how it occurs
Describe how the concentration of calcium must change over an action potential and release of an NT
In order for the NT to be released,, the concentration of calcium in the presynaptic terminal must rise after the action potention, in order for the synapse to transmitt signals at high frequency the terminal must return to resting state quickly after NT release so the [Ca] must be brough back down
List the 4 steps invovled in NT vesicle exocytosis
1. vesicle moves to the active zone
2. proteins attach the vesicle to the active zone
3. SNARE proteins dock vesicle to membrane
4. fustion between vesicle and membrane when [Ca2+] increases
what is nonspiking release?
Some neurons never carry APs but rather release NTs in response to electrotronic voltage signals, the amount of NT released depends on Vm which controls the activity of the voltage gated Ca2+ channels
what are some benefits of electrical synaptic transmission
fast, faithful, bidrectional, used when many cells need to fire synchronously such as in cardiac muscle
How is calcium able to move into the presynaptic cell and assist with NT release
the action potential generated in the presynaptic cell moves to the nerve terminal and opens the voltage gated calcium channels
how do NTs travel across the synaptic clef?
diffusion
What does binding of an NT to a post synaptic membrane generate
an ipsp or an epsp, may or may not cause an action potential
How can a neurotransmitter be removed from the synaptic clef
enzymes, transport proteins that take it back into the presynaptic cell, degradation by glial cells
what proteins are responsible for trafficking NTs to the active zone
actin and myosin
Compare and contrast how fast and slow chemical synapses open the ion channels
fast synapses open the channes directly because they are ligand gated, slow synpases open the channels via 2nd messenger action (phosphorylation of the channel, transcription factor changes synthesis of ion channel protein, etc)
How do the signaling molecules differ between fast and slow chemical synaptic transmission
fast- small molecules
slow- large molecules
Describe an excitatory synapose
influx of positive charge depolarizes the membrane, increase of sodium and potassium permeabiltiy or increase of calcium permeabilty in the postsynaptic membrane
what ions are invovled in inhibitory synapses
potassium or Cl-
what propery eventually allows ipsps or epsps to generate action potentials
summation, the small changes in potential caused by each ipsp or epsp to add up and eventually cross the threshold for generation of an AP
which Ach receptor causes epp at the neuromuscular junction
nicotinic