The action potential

Question 1

Membrane potential is measured as the potential of the extracellular solution relative to the inside of the cell, is this correct?

Answer 1

No! Membrane potential is measured as the potential inside the cell relative to the extracellular solution

Question 2

What unit are membrane potentials measured in?

Answer 2

Millivolts mV

Question 3

Which cells have membrane potentials at rest and are they positive or negative?

Answer 3

All animal cells do- they are negative

Question 4

What two factors are important for the generation of the membrane potential?

Answer 4

Asymmetric distribution of ions across the plasma membrane

Selective ion channels in the plasma membrane

Question 5

Electrical gradient has more effect on direction of ion flow than concentration gradient, is this correct?

Answer 5

No, ions will always move down their concentration gradient first and then down their electrical gradient.

Question 6

What is equilibrium potential for an ion?

Answer 6

The membrane potential if it solely relied on that ion.

Question 7

What is the nernst equation?

Answer 7

A way for working out equilibrium potential-

E=61/charge on ion multiplied by log (concentration of ion on outside/concentration of ion on inside)

Question 8

What is depolarisation?

Answer 8

A decrease in the size of the membrane potential from its normal value so cell becomes less negative

Question 9

What is hyperpolarization?

Answer 9

An increase in the size of the membrane potential from its normal value so the cell become more negative

Question 10

What will increasing membrane permeability for a particular ion do to the membrane potential in regards to the equilibrium potential of that ion?

Answer 10

It will move the membrane potential towards the equilibrium potential of that ion.

Question 11

What are changes in the membrane potential caused by?

Answer 11

Changes in membrane permeability due to changes in activity of ion channels.

Question 12

What is conductance?

Answer 12

The contribution of each ion to the membrane potential will depend on how permeable the membrane is to that ion.

Question 13

Which equation can we use that takes into account imperfect selectivity of each ion? What must you remember to do?

Answer 13

The GHK equation, turn the logarithmic fraction for chloride ions upside down.

Question 14

What are the different ways a cell can be gated?

Answer 14

Ligand gating
Voltage gating
Mechanical gating-membrane deformation causes opening or closing of channels

Question 15

How is mechanical gating used in the inner ear?

Answer 15

K+ channels close in the cuticular plate, this causes the membrane to depolarise. This causes calcium ion channels to open.
Vesicles containing neurotransmitter fuse with the basement membrane close to the afferent nerve
Neurotransmitter binds to receptor on post synaptic plate and generates action potential that goes to CNS for interpretation

Question 16

What is the receptor protein in fast synaptic transmission?

Answer 16

An ion channel- neurotransmitter binding causes the channel to open.

Question 17

How do inhibitory synapses work? What are some common inhibitory neurotransmitters?

Answer 17

Opening of ligand gated channels which cause hyperpolarization
Common neurotransmitters include-glycine, GABA

Question 18

Which two ways can slow synaptic transmission work?

Answer 18

Direct G protein gating

Gating via an intracellular messenger

Question 19

How does direct G protein gating work and what are its benefits?

Answer 19

Binding of signal chemical to GPCR causes release of G protein which then moves along the inside of the membrane and binds to channel- hydrolyses ATP and opens channel

This is localised and quite rapid

Question 20

How does gating via an intracellular messenger work and what are its benefits?

Answer 20

G protein activation causes enzyme activation which initiates signalling cascade which activates intracellular messenger or protein kinase which opens channel.

This happens throughout the cell as it is not confined to the plasmalemma
The signal can be amplified by cascade
However is slow as more intermediates

Question 21

What are the different stages of the action potential in cardiac muscles?

Answer 21

1-rapid influx of Na+ through open fast na+ channels
2-transient K+ channels open and K+ efflux returns membrane potential to 0mV

3. Influx of calcium through L type calcium channels is electrically balanced by K+ efflux through delayed rectifier K+ channels
4. Calcium ion channels close but delayed rectifier K+ channels remain open and return membrane potential to -90mV

Question 22

What are the properties of cardiac ion channels?

Answer 22

Selectivity-only permeable to a single type of ion
Voltage sensitive- a specific MP range is required for particular channel to be in open configuration
Time dependent- some ion channels are configured to close a fraction of a second after opening (become inactivated and can only be opened again when the MP is returned to resting levels.

Question 23

What is the part of the axon at which membrane potentials ‘sum up’ to possibly create an action potential?

Answer 23

The axon hillock

Question 24

Why is there such a rapid increase in membrane potential during the action potential?

Answer 24

Positive feedback loop for sodium
Sodium influx causes membrane depolarisation which causes more sodium channels to open which causes more influx so more depolarisation.

Question 25

Why does the membrane potential stop rising?

Answer 25

All sodium channels have become inactivated.

Question 26

What is the difference between the absolute refractory period and the relative refractory period?

Answer 26

Absolute- no action potentials can be stimulated- all sodium channels inactive relative- an AP can be produced if the stimulus is large enough, some sodium channels have started to recover

Question 27

What is the structural difference between sodium and potassium channels?

Answer 27

Both have four subunits each made up of 6 transmembrane regions. Sodium transport proteins contain an inactivation particle which blocks the pore and inactivates the channel. Sodium channels are also made of only one alpha subunit. Potassium channels are made up of four alpha subunits.

Question 28

What is the local current theory?

Answer 28

Injection of current into an axon will cause the resulting charge to spread along the axon and cause an immediate local change in the membrane potential- this spreads according to an inverse exponential graph

Question 29

What is capacitance?

Answer 29

The ability to store charge and is a property of the lipid bilayer

Question 30

What controls the membrane resistance?

Answer 30

The number of ion channels open.

Question 31

What effect will a high capacitance have on voltage change?

Answer 31

Voltage will change more slowly in response to current injection

Question 32

What effect will a higher resistance have on how far the change in voltage spreads along the axon?

Answer 32

It will spread further- this is why myelination increases distance each action potential 'covers'

Question 33

What do i need to know about voltage gated calcium channels?

Answer 33

Similar to sodium channels- different depending what organ they are in Activate more slowly than sodium channels Also activate and inactivate Inactivation in calcium ion dependent.

Question 34

How is neurotransmitter released from the presynaptic neurone?

Answer 34

``` Calciu enters through channels when stimulated by depolarisation Calcium binds to synaptotagmin Vesicles brought close to membrane Snare complex makes a fusion pore Transmitter released through pore ```

Question 35

What happens when neurotransmitter binds to receptors on the post synaptic membrane?

Answer 35

Brief depolarisation will activate adjacent sodium voltage gated channels due to local spread of charge.

Question 36

How are ligand gated ion channels on the post synaptic membrane different?

Answer 36

They allow both sodium and potassium through. However more sodium will move in because the membrane potential is further away from the Ena. Than from the Ek

Question 37

How does tubocurarine work?

Answer 37

Competitive inhibitor of Ach binding sites on ligand gated ion channels so less opening- less depolarisation of post synaptic neurone

Question 38

How does succinylcholine work?

Answer 38

Brief depolarisation activates then deactivates vg sodium channels. Because SC not degraded by Ach esterase it stays in receptors and continues to cause depolarisation so voltage gated sodium channels stay inactivated.

Question 39

What is mayasthenia gravis?

Answer 39

Autoimmune disease targeting nACh receptors Patients suffer profound weakness Weakness increases with exercise Caused by antibodies directed against nAChr on post synaptic membrane of skeletal musclethis leads to loss of functional nAChR by complement mediated lysis and receptor degradation Endplate potenitals are reduced in amplitude therefore leading to muscle weakness and fatigue

Question 40

How does a muscarinic Ach receptor operate differently from a nicotinic receptor?

Answer 40

Produces a slower depolarisation because they are coupled to G proteins which trigger a cascade of events in the cell.