Action Potential And Propogation Notes

Action potential propagation

Action potential

Propagating, regenerative, transient, all or nothing depolarisation-Transient electrical impulse which causes the membrane potential to be displaced about 100mv -caused by rapid changes in the membrane permeability to sodium and potassium overtime.

-only occur in electrically excitable cells as these only possess voltage activated ion channels

-information is carried by the frequency of action potentials as the amplitude remains the same

Mechanism for action potential generation

-In an exam always begin by drawing the action potential diagram-

Voltage clamp theory

-2 electrodes are inserted into the cell, one for monitoring the Em, one for injecting current

-When voltage sensing electrode detects a difference from the intended voltage, commonad voltage, feedback amplifier injects opposing current to maintain Vm-magnitude of the total injected current is equal to the total membrane current

I membrane = I ionic current + I capacitative current

-The flux of potassium and sodium was shown using the voltage clamp theory which measures the current of both sodium ions and potassium ions across the membrane. Imembrane = I channel + I capacitance (due to electrodes) Upon depolarisation due to the capacitative current, in addition to the capacitative current there is also large inward time dependent ionic current into the axon due to sodium ions shown using tetrodoxin. The inward current is then followed by outward current which is due to potassium ions shown using tetraethylammonium

-important, must say in exams: the advangtage of using the voltage clamp theory is that the voltage current eliminates the capacity current and prevents it interfering with the channel current.

Stages of action potential

-stimulus such as a synaptic input/ chemical or physical stimuli caus

es a local depolarisation- by the opening of cation channel- small increase increase in Em. If the depolarisation causes the membrane to reach a threshold potential it stimulates an action potential.

Threshold: the voltage at which an action potential is triggered. Occurs when the influx of sodium ions through volgate gated sodium channels exceed the efflux of background potassium ions through the leak channels- there is net inward current

-opening of voltage gated sodium ion channels, which leads to the influx of sodium ions into the membrane, depolarises the membrane further and leads to more voltage gated sodium ion channels opening- this positive feedback loop leads to a rapid positive increase in the membrane potential- leads to upstroke of the action potential

Evidence that action potential is dependent on Na- giant squid axon fails to generate an action potential in a sodium ion free solution and there is graded reduction in the overshoot of AP

-after a certain time- the voltage gated sodium ion channels become inactivated- the permeability of the sodium ions returns to resting value- less positive ions enter- beginning of repolarisation -using the voltage clamp theory, when the potassium current was blocked and the sodium current was measured it showed that the current decreased over time, shown voltage gated ion channels existed in three conformations: closed, open and inactive state

- in an inactivated state Na can’t pass through, it is distinct from the closed channels as they can’t reopen until they recover from inactivated state which is voltage dependent and will not occur until the membrane is repolarised- so recovery from inactivation is time dependent-Some drugs bind to specific states- lidocaine, local anaesthetic binds to inactivated states of sodium, drug is more sensitive on sodium ion channels that are more active- this is effective as it targets pain first

- also contributing to repolarisation -the voltage gated potassium ion channels, delayed rectifier potassium channels open. The depolarisation of the membrane leads to the opening of both sodium and potassium but as the potassium ion channels have slower kinetics they ony open once the voltage gated sodium ion channels close- the opening of the voltage gated potassium ions leads to the efflux of potassium ions- brings Em closer to Ek.

-voltage gated sodium ion channels need a smaller depolarisation to open compared to voltage gated potassium ion channels and this leads to a time delay in the activation of sodium and potassium- see graphs on (important graphs to draw in exams page!)

-this repolarises the membrane and makes the membrane more negative- this has a negative feedback effect and causes voltage gated potassium ion channels to close- but as the channel has slow kinetics- it leads to the membrane becoming hyperpolarised- more negative than resting Em

-once repolarisation has occurred sodium ion channels recover from inactivation

Important toxins that can inhibit the formation of an action potential – shows the role of Na/K

-tetrodotoxin- blocks voltage gated sodium channel- acts on the extracellular side of the cell membrane –allows us to study the permeability of potassium ion channels independently to sodium ions

-tetraethylammonium ions- block potassium channels

-using the voltage clamp theory it was shown the current voltage relationshipsfor voltage gated sodium and potassium channels in the nerve

-another cause for action potential which leads to contraction in cardiac cells and smooth muscle cells are voltage gated ion channels- open and close more slower which leads to action potentials that lase for longer

Restoring ion concentrations

This is done due to sigmoidal activity of Na⁺/K⁺ ATPase in response to changes in local intracellular Na⁺ concentrations at physiological changes: e.g. when Na⁺ goes from 10mM to 20mM activity increases 8x. This may not be over the whole cell, but just in the local environment of the channel. This proven experimentally by increased heat generation due to increased ATP production

Refractory period

-absolute refractory period is the period of time when an action...

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