Action Potentials

how long does an action potential typically last?

1-2 milliseconds

where do action potentials typically occur?

excitable cells (neurons, muscle cells, cardiac cells, endocrine cells), which are cells with negative resting membrane potential

what is the action potential threshold?

the membrane potential where the AP starts

what is the structure of voltage-gated Na+ channels?

a single large alpha subunit, that forms an ion-conducting pore- with voltage sensors. ( comprised of 4 domains, each containing 6 transmembrane segments- with voltage sensors on the 4th transmembrane segment )

what is the 4 key features of a voltage-gated Na+ channel?

1. selectivity filter (for Na+)
2. a voltage sensor
3. an activation gate
4. an inactivation gate

what does 1 voltage-gated Na+ channel opening, and Na+ moving down it's concentration gradient into the cell, result in?

a chain reaction from the region of positive charge across the membrane, causing more voltage gated Na+ channels to open- leading to depolarisation

what happens to voltage-gated Na+ channels following activation?

they rapidly inactivate via the inactivation gate closing/blocking Na+ flow

when do voltage-gated K+ channels activate?

following voltage gated Na+ channels closing

how do voltage-gated K+ channels work in comparison to voltage-gated Na+ channels?

voltage-gated K+ channels are also activated by depolarisation but activate more slowly than voltage-gated Na+ channels

what does K+ leaving the cell result in?

hyperpolarisation

what maintains the resting membrane potential?

leak K+ channels

describe the 4 stages of an Action Potential

1. resting membrane potential is maintained by leak K+ channels
2. when membrane potential reaches threshold, voltage gated Na+ channels open/activate- leading to more vgNa+ channels to open causing depolarisation
3. Na+ channels inactivate and (slower) vgK+ channels activate leading to hyperpolarisation
4. vgK+ channels can cause an 'overshoot' called afterhyperpolarisation- but eventually resting membrane potential is re-established

within the axon, what makes electrical resistance higher?

the thinner the axon, the slower the conduction signal

what does the myelin sheath insulate the axon against?

external negative charge, allowing faster transmission

why do action potentials degrade?

myelinated axons still have some capacity to store charge (carried by +ively charged ions)

how do nodes of Ranvier act as signal boosters?

they have high density of vgNa+ and vgK+ channels, when an action potential meets a node of Ranvier: it initiates a new actin potential (hence why the original AP doesn't degrade)

what contributes to threshold differences of a cell?

the activation properties of vgNa+ channels

why are activation threshold differences important?

for example, if more negative, takes more depolarisation to reach threshold ( can effect firing frequency )

what are the 3 states of a vgNa+ channel?

1. closed
2. open.
3. inactivated

how does a vgNa+ channel open and close?

must cycle from open activation gate, to inactivation gate closing, then the activation gate closes after- must go in a cycle

what does recovery from inactivation depend on for vgNa+ channels?

the voltage steps (ie more depolarised potential between pulses of AP)