2.7 (2) Action Potential (Dr. Talbot)

Know the basic terminology associated with changes in membrane potential $$$ (Resting potential, Hyperpolarization, Depolarization, Threshold potential, AP, Graded potential)
1.) Resting potential = potential maintained across membrane of excitable cells (neurons, muscle)

2.) Hyperpolarization = Vm more negative than rest

3.) Depolarization = Vm less negative (or positive) than rest

4.) Threshold potential = the level of depolarization that triggers an AP

5) Action potential = a rapid, large regenerative depolarization; it is a process and describes a change over time.
Depolarizing stimulus of sufficient intensity induces AP
voltage-gated ion channels
– NO decay

6) Graded potential = Amplitude of voltage deflection is variable and dependent upon stimulus intensity.
– Magnitude of voltage deflection proportional to rate of current flow.
– Can occur along axonal domain as long as depolarization is less than threshold
– Decay

Know the different membrane domains in the neuron, the types of channels present in each domain and how opening of those channels affects Vm $
1) Somatodendritic domain (basal)
– cell body & dendrites
Ligand-gated ion channels & GPCRs
Graded response – passive spread

2) Axonal domain (apical)
– axon
Voltage-gated NaK ion channels
All or none response
AP starts at axon hillock!

Know the ionic basis of an action potential in a neuron
– Conduction signal at axon hillock -> opens voltage-gated channesl -> Na+ rushes into cell and depolarizes membrane

What are the requirements for cells to generate an action potential?APs REQUIRE:
1) *Presence of voltage-gated Na+ and K+ channels
2) Maintenance of resting Vm (-)

– Function of Vm change over time

Know which ion channels are responsible for which parts of the action potential profile
1) Resting state: ALL voltage-gated Na+ and K+ channels closed

2) Depolarization phase: voltage-gated Na+ channels open, INCREASE in Na+ permeability (Na+ rushes in)

3) Repolarization phase: voltage-gated Na+ channels inactive and K+ channels open (K+ exits)

4) Hyperpolarization phase: K+ channels slowly close and Na+ channels transition from inactive back to closing

NB: – Voltage-gated Na+ channels open quickly, inactivate quickly. Voltage-gated K+ channels open slowly, inactivate slowly. – Not just change in Vm that induces response but the response of an entire population of channels

K= koala = slow creatures

What is inactivation and why is it important? Know how inactivation relates to the refractory period.
Inactivation of voltage-gated Na+ channels means that channel is unable to respond to depolarization (change in Vm). It is voltage insensitive.

Relation to refractory (unresponsive) period: Inactive voltage-gated channels ensure refractory periods (membranes unresponsive to further depolarizations)

– Two gates in voltage-gated Na channel: voltage sensitive gate and inactivation particle
– Closed voltage-gated Na+ channels are voltage sensitive
Absolute refractory period – no AP EVER.
Relative refractory period – smaller than normal heigh AP possible (and requires a larger than normal stimulus)
Magnitude of AP is a function of the number of Na+ channels that are open

Know how positive feedback is used to help develop an action potential (Hodgkin Cycle)
Hodgkin Cycle
– Example of positive feedback– depolarization reinforced
– Any stimulus that depolarizes membrane enough above threshold that causes voltage-gated Na+ channels to open will further cause other neighboring Na+ to open.

Outside mechanism = spontaneous inactivation of the channels

– Depolarization in one place will cause depolarization in another

Know how action potentials are propagated down an axon
1) Passive spread of depolarization – change in Vm spreads in all directions from point source without requiring proteins (electronic spread) but magnitude decreases with distance.

2) AP propagate down an axon without decay – stimulus above threshold will create AP that propagates w/o decay bc a new AP is regenerated at each point along the membrane (Amplitudes constant and maximal)

3) Nodes of Ranvier and Myelin Sheath move AP by saltatory conduction – AP regenerated at each node as Vm depolarizes again
Clinical: MS attacks myelin sheath

What affects velocity of conduction?What affects the velocity?
1) Axonal diameter – the larger the diameter, the lower the cytoplasmic resistance
2) Whether axon is myelinated or not (by Schwann cells) More myelinated axon = increased membrane resistance

Passive spread of change in potential governed by:
1) Shape of cell
2) Resistance to ion flow across membrane and cytoplasm (Length constant directly related to membrane resistance, inversely related to resistance of cytoplasm) Rmem generally > Rcyto
3) Capacitance of membrane

NB: Length constant determines how far signal will move before decay from max value by 63%

TTX (Tetrodotoxin)
Blocks fast voltage-gated Na+ channel of neurons and striated muscle. Hyperpolarization will occur at that single point but single will not be propagated.
Other important points– AP doesnt get generated until we get to axon hillock
– K+ efflux will always cause inhibitory post synaptic potentials (IPSP)
– Cl is usually inhibitory PSP
– NA+ influx -; EPSP
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