32. Action Potentials Flashcards
Can you describe the action potential travelling along a mixed nerve?
Diagram page 99
The term action potential describes
the depolarisation above threshold potential,
+ subsequent repolarisation - a nerve axon resulting in
propagation of a nerve impulse along that axon.
The easiest way to describe this is in a series of steps relating to the diagram of the AP:
- > The inside of each cell in the body is negative
relative to its surroundings.
The potential difference
= membrane potential (Em)
-governed by the membrane’s relative permeability
to sodium (Na+) and potassium (K+) ions.
When the cell is at rest, it is relatively more permeable to K+ than Na+
and so the resting membrane potential approaches the equilibrium potential of K+.
In a mixed nerve this Em is −70 mV.
- > Nerve, muscle cells and pacemaker cells are able to generate APs.
When a stimulus causes a movement of charge across the membrane, there is a movement away from the resting membrane potential.
If the inside of the cell becomes more positive = depolarisation
more negative, = hyperpolarisation.
Depolarisation in a nerve cell is caused by the
movement of Na+ ions into the cell.
3.
If a nerve cell becomes depolarised,
e.g. by distortion opening Na+ channels in the mechanoreceptors of the skin,
the movement of the membrane potential towards zero causes opening of voltage-gated Na+ channels.
Once a Na+ channel opens, it will close again automatically after a millisecond or so.
Therefore, if the initial stimulus is not strong enough to cause enough Na+ channels to open to allow enough Na+ into the cell to bring the Em to threshold potential, the membrane potential will fall away from zero and become more negative as the K+ equilibrium
is re-established.
Consequently, no AP will be generated.
- > If, however, the initial stimulus is strong enough, enough channels will open
- allow an influx of Na+ that will
raise the membrane potential to the threshold level of −55 mV.
If this level is reached,= positive feedback effect occurs on the Na+ channels,
causing large numbers of them to open.
Consequently, there is an explosive influx of Na+ raising the membrane potential above 0 to +35 mV.
So, the AP is an ‘all-or-nothing’ event –
the membrane either reaches threshold level or
does not.
- > These Na+ channels opened by positive feedback will still close rapidly, as before.
As the membrane potential nears the equilibrium potential of Na+ (+70 mV),
the diffusion of Na+ ions into the cell slows.
The maximum membrane potential is defined by the relationship of the Na+/K+ equilibrium
, therefore, the size of the AP is fixed, and not dependent on the size of the stimulus.
Similarly, the duration is fixed, because this is dependent on the length of time that the Na+ channels remain open, and this time is fixed.
- > Once the Na+ channels close,
repolarisation occurs
by the movement of K+ ions out
of the cell to restore the resting membrane potential.
This happens as voltage-gated K+ channels open in the face of an AP, allowing the movement of the K+ out of the cell along its diffusion gradient.
These K+ channels remain open after the Na+ ones have closed,
= resting membrane potential to be re-established.
This process is called delayed rectification.
Following only a few APs, the net change in number of Na+ and K+ ions in and outside the cell is small.
However, after many APs, the changes become
significant and the balance across the membrane is restored using the Na+-K+ pumps.
- > An inactivated Na+ channel cannot reopen
until it has returned to near resting membrane potential.
This explains the absolute refractory period
that follows each AP,
where the nerve cell cannot be excited,
no matter how large the stimulus.
The relative refractory period follows the absolute
refractory period, and here, another AP can be generated with a supramaximal stimulus.
How does the AP move along the axon of a nerve?
In an unmyelinated axon the AP moves rather like a wave;
local currents spreading in front of the AP cause a change in membrane potential and
bring the membrane to threshold potential to spark the propagation of the AP.
The AP can only flow in one direction as the axon behind it will be refractory.
Myelin acts as insulation because the
charge cannot leak from the
axon in an area covered by the myelin,
and so charge density is maintained.
In the ‘nodes of Ranvier’,
i.e. the spaces between the myelinated areas,
the charge can escape; t
he net effect is that the AP jumps from node to node. This is called saltatory conduction.
So, the myelin increases the AP’s velocity, and its insulating effect allows axons to be of smaller
diameter (without myelination, conduction is fastest in axons with larger diameters)
What is the Gibbs–Donnan equilibrium?
‘Diffusion of permeable ions across a semipermeable membrane down their concentration gradient is balanced by the electrostatic attraction of impermeable ions (e.g. proteins) trapped on the inside of the membrane
What is the Nernst equation?
The Nernst equation calculates
the electrical potential for an individual ion,
thus helping to predict how
each ion affects the cell membrane potential.
It represents the electrical potential
required to balance a given ionic
concentration gradient across a membrane
so that there is no net flux.
Em =
RT
___
ZF
[ion]OUT × In \_\_\_\_\_\_\_\_\_
[ion]IN
Where:
[ion]OUT
Extracellular concentration of that ion
(in moles/cubic metre)
[ion]IN
Intracellular concentration of that ion (in moles/cubic metre)
Em Membrane equilibrium potential
R Universal gas constant
T Absolute temperature
Z Valency
F Faraday’s constant
Because R, T and F are constants and Z is 1 for the majority of ions in
which we are interested, the Nernst equation can be simplified to:
[ion]OUT Em = 61.5 × log10 \_\_\_\_\_\_\_\_\_
[ion]IN
What is the Goldman constant
field equation?
This calculates the value of the overall membrane potential taking into account the permeabilities and concentration gradients of each ion.
eqn page 101
Vm = Membrane potential R = The permeability of that ion (in meters/second)
