Revision 4: Electrical Excitability

Question 1

Properties of an AP

Answer 1

1 change in voltage across a membrane

2 All/nothing

3 propograted w/o loss of amplitude

4 depends on ion gradients and relative permeability

5 only occurs if threshold is reached

Question 2

Changes in membrane ionic permeability in, and the ionic of, an action potential

Answer 2

Once the threshold potential is reached, Na⁺ VGCPs open and Na⁺ floods into the cell, attempting to reach its Equilibrium potential of +61mV

-> this causes increased depolarisation, leading to more Na⁺ VGCPs opening, leading to more depolarisation etc

As the membrane potential reaches +40mV, Na⁺ channels close by inactivation, so Na⁺ influs stops -> repolarisation

-also, K⁺ VGCPs open, K⁺ moves out -> repolarisation

Question 3

describe basis of All/nothing, Refractory periods, and accommodation

Answer 3

A/N: Na⁺ channels are VG -> +ve feedback ensures that more channels will open until they all are

RPs: Absolute: Nearly all channels are inactivated, excitability is 0, cannot be stim.

-Relative: Na⁺ VGCPs are recovering from inact., can be stimulated but need bigger stim. as excitability is lowered

Accommodation: the longer the stimulus, the larger the depol. needed to initiate an AP, as more Na⁺ channels have been activated

Question 4

Ion channel properties

Answer 4

VGNa⁺/Ca²⁺CPs: 1 peptide, 4 homologous repeats, in each subunit there are 6 transmembrane domains (1 is voltage sensitive), function needs 1 subunit

VGK⁺CPs: 4 peptides, Function needs 4 subunits, 6 transmembrane domains, 1 is voltage sensitive

Question 5

Local anaesthetics mode of action

Answer 5

eg lidocaine, procaine

Bind to and block Na+ channels, stopping AP generation

Block conduction in: 1 small myelinated then 2 nonmyelinated then 3 Large myelinated axons

Therefore tend to affect sensory before motor functions

Two pathways: Hpho/no use dependence: no charge on the ion, enters PM and blocks the channel from inside, by binding to an H+ from inside the channel

-Hphi/use dependence: moves across PM into cell, binds to H+, enters channel and blocks it when opened

Question 6

Measuring conduction velocity

Answer 6

EC recording: electrodes are used to raise the PM potential to threshold to generate an AP, by recording changes in potential between the stimulating (-ve) and recording (+ve) electrodes along an axon, the conduction velocity can be measured as Distance/Time

Question 7

local current theory

Answer 7

Depol. of small region of membrane -> transmembrane currents in neighboring regions -> opens more VGNa⁺CPs -> propogation of AP

the further the local current spreads, the faster the conduction velocity of the axon

Question 8

Properties that lead to a high conduction velocity

Answer 8

Ohm’s law is V=IR

1 High membrane resistance: higher the resistance, the higher the voltage -> inc. VGCPs opening -> threshold reached more easily and conduction velocity inc.s

2 large axon diameter: dec. cytoplasmic resistance -> dec. resistance -> inc. current -> AP travels further -> conduction velocity inc.s

3 Low membrane capacitance: capacitance is the ability to store charge, so less current/time is needed to charge the membrane

Question 9

Implications of myelination for conduction, how it works, where they are found and synthesis

Answer 9

Rapidly inc.s conduction velocity

Large diameter axons eg motor neurones are myelinated whereas smaller ones eg sensory neurones are not

Effect: dec. capacitance and inc. membrane resistance -> inc. conduction velocity, also saltatory conduction is induced, where the AP jumps between nodes of Ranvier, which have a greater density of VGNa+CPs

schwann cells myelinate peripheral axons, oligodendrocytes myelinate central axons

Question 10

consequences of demyelination

Answer 10

eg MS - AImm. disease, myelin is destroyed in certain areas of CNS

dramatic effect on ability of previously myelinated axons to conduct APs correctly -> dec. conduction velocity/complete block/intermittent transmission

• Immediately: Conduction failure due to increased neuronal membrane capacitance and current leak preventing nodally distributed channels from being raised to threshold
• After a period of recovery: Re-establishment of nerve impulses with slower conduction velocity due to the redistribution of nodal ion channels in the nerve membrane (effectively becomes an unmyelinated nerve)