Action Potential Flashcards
1
Q
Active signals in nerve cells
A
- a stimulating and a recording microelectrode are inserted into a neuron
- the lower panel shows potential recorded drops from zero to -65 mV
- current pulses are then passed by the stimulating electrode (upper panel), first hyperpolarizing (first two pulses)
- the second depolarizing pulse depolarizes the membrane to threshold producing a brief spike of depolarization called an action potential
- great depolarization produces more spikes at higher frequency
2
Q
Phases of the action potential
A
- rising depolarizing phase
- falling repolarizing phase
- the undershoot or afterhyperpolarization phase contains a refractory period during which it is not possible for the axon to have an action potential and then a relative refractory period when it required greater stimulation for the axon to produce another AP
- the undershoot then dissipates and the membrane potential returns to resting
3
Q
The rising depolarizing phase of the action potential
A
- experimental verification that Sodium is essential for the generation of AP
- lowered external NA+ results in smaller and slower action potentials
- sodium channels contribute to the depolarizing phase
- an important control is to return the external solution to normal
4
Q
Voltage sensitive mechanisms during the action potential
A
- action potentials are generated by three different voltage-sensitive mechanisms:
- 1) activation of Na+ conductance
2) delayed activation of K+ conductance
3) inactivation of Na+ conductance - the undershoot of the membrane potential is due to open voltage gated K+ channels that gradually close and the membrane potential returns to the resting membrane potential
5
Q
Activation of Na+ conductance
A
- the voltage-depedent Na+ channels open and Na+ ions rush into the cell down their concentration gradient (inward current)
- accumulation of + charge inside and across the cell membrane
- depolarization of the membrane potential
6
Q
Delayed activation of K+ conductance
A
- after a delay the voltage-dependent K+ channels open
- K+ ions rush out the cell down their concentration gradient (outward current)
- reduction of + charge inside the cell membrane
- hyperpolarization of the membrane potential
7
Q
Inactivation of Na+ conductance
A
- voltage-dependent Na+ channels transition to a non-conductive state as voltage gated K+ channels begin to close
- the cell is refractory and does not fire action potentials in response to stimulation
- the inactivation gates then begin to open and the Na+ channels close
8
Q
Voltage Clamp Approach
A
- varied the membrane potential in squid giant axon to measure the changes in membrane conductance through voltage gated Na+ and K+ channels
- to interrupt the positive loop between membrane potential depolarization and the opening and closing of voltage gated channels
- the voltage clamp amplified injects a current into the cell that is equal and opposite to the current flowing through the voltage gated channels
9
Q
Changes in Na+ and K+ conductance
A
- the voltage clamp technique reveals two types of voltage dependent ion currents
- an early inward current (Na+)
- a late outward (K+) one
- the capacitive current supplies charge for the change accumulation across the membrane needed to step from a holding membrane potential to the new membrane voltage
10
Q
Drugs that change Na+ and K+ conductance
A
- using the voltage clamp technique it was shown that drugs that selectively block Na+ and K+ currents also selectively block the early and late currents
- TTX (tetrodotoxin) blocks sodium channels without affecting K+ channels- from puffer fish
- TEA (tetraethylammonium bromide) blocks K+ channels and is also an ACh receptor blocker
11
Q
Action potential propagation
A
- AP conduction required both active and passive current flow
- active- the gating of voltage gated channels and associated influx of Na+ current
- passive- depolarization wave the precedes the AP, positive ions entering axon via electrode or activated Na+channels passively move down the axon and neutralized negative membrane charges, decreasing the capacitive charge on the membrane and driving the membrane potential to threshold
- there is no passive current flow through the membrane only through channels
- passive positive ionic flow that neutralizes the negative charges on the inside of the membrane discharging the membrane capacitance and leading to sodium channel activation
- can only go the one direction because other side is inactivation
12
Q
Relative refractory period
A
-brief hyperpolarized membrane potential due to open resting and voltage gated K+ channels that ends when the voltage gated K+ channels close
13
Q
Summary changes in Na+ and K+ conductances
A
- Hodgkin and Huxley used the Voltage Clamp Technique to determine that Na+ and K+ conductances change with time and membrane potential
- APs are generated by four mechanisms: activation of Na+ conductance, activation of K+ conductance, inactivation of Na+ conductance, closing the voltage gated K+ channels
- APs first reverse the sign of the membrane potential at the peak (overshoot; gNa increase) and then hyperpolarize the membrane potential (undershoot; gKincrease) yielding a refractory period during which it is impossible, then harder (relative refractory) for the axon to produce another AP. Undershoot the dissipates (gKdecrease) and membrane potential returns to normal
14
Q
Myelination
A
- wrapping of glial cell membranes around the axon
- functionally equivalent to increasing membrane thickness by 100 times
- increases insulation which reduce leak of passive flow
- also decrease capacitance -> C= EA/d (d is total thickness, A= area)
- Na+ and K+ ions are localized
15
Q
Conduction in myelinated nerves
A
- fast passive potential between the nodes of Ranvier
- generation of action potential in the nodes (boosting stations)
- saltatory conduction: APs jump from node to node
16
Q
Nodes of Ranvier
A
- gap in myelin sheath
- separated by 1 or 2 mm
- contain full complement of Na+ and K+ channels
- generate action potentials
17
Q
Conduction velocity of nerves
A
- unmyelinated: 0.5 to 10 m/s
- myelinated ~150 m/s
18
Q
Multiple sclerosis
A
- a demyelinating disease, disrupts saltatory conduction slow and even blocking the transmission of nerve impulses in the CNS
- demyelination increases the capacitance of the membrane and thereby slows or even blocks AP propagation
- capacitance of node is 100-200 times greater than that of the intermode in normal nerve
