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ICPP > Membrane Potential > Flashcards

Membrane Potential Flashcards

1
Q

What are the causes of the membrane potential?

A

Unequal distribution of ions

Selective ion channels

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2
Q

What is the equilibrium potential for an ion X?

Definition and Equation

A

Membrane potential at which X will be in equilibrium (no net movement), given the concentration of X outside and inside the cell
Ex=(RT/ZF)*ln(C2/C1)

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3
Q

If a membrane is selectively permeable to X only what is it’s membrane potential?

A

Membrane potential = Ex

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4
Q

Define: Depolarisation
Hyperpolarisation
Depolarisation

A

Depolarisation: Membrane Potential becomes less negative
Hyperpolarisation: Membrane Potential becomes more negative
Repolarisation: Membrane Potential becomes less positive

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5
Q

What are the characteristics of the Action Potential?

A

Only occur when the threshold potential is reached

Propagated without loss of amplitude

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6
Q

What happens to the membrane potential when the cell membrane becomes more permeable to an ion?

A

Membrane potential moves closer to the equilibrium potential of that ion

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7
Q

Define conductance

A

How permeable a membrane is to a particular ion (and how much that ions equilibrium potential contributes to the membrane potential)
Depends on the number of ion channels for that ion

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8
Q

What are the types of gated ion channels?

A

Ligand (binding of another molecule)
Voltage (change in membrane potential)
Mechanical (membrane deformation)

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9
Q

What is the differences between fast and slow synaptic transmission?

A

Fast: the receptor is the ion channel
Slow: the receptor and ion channel are separate
Both use ligand-gated ion channels to change selectivity of the membrane to certain ions

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10
Q

Describe the types of fast synaptic transmission

A

Excitatory: binding causes depolarisation
Inhibitory: binding causes hyperpolarisation
Fast synaptic transmission has a longer time course than action potential (based on the concentration of ligand)

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11
Q

Describe the types of slow synaptic transmission

A

GPCR: activates G-Protein which bind to receptor (quite rapid, localised)
Intracellular messenger: messengers formed from the action of enzymes bind to receptor (ubiquitous, can cause amplification cascade)

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12
Q

Describe the stages of the action potential

A

Change in the Membrane Potential (depolarisation)
Once Membrane Potential reaches threshold potential, Voltage-gated Na+ channels open
Causes an influx of Na+ into the cell and further depolarisation
When the membrane potential reaches its peak (Na+ channels become saturated) the Na+ channels inactivate and the K+ channels open slowly
K+ starts to leave the cell
This causes repolarisation and the membrane potential starts to return to its resting potential
When the membrane potential reaches its resting potential the K+ channels close slowly leading to hyperpolarisation

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13
Q

Describe the features of the Na+ channel:

A

1 alpha unit (4 subunits linked together)
6 transmembrane domains in each subunit
S4: positively charged voltage-sensing domain
S5-S6: pore forming domain (channel)
Between the 3rd and 4th subunit is the Inactivation gate

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14
Q

Describe the features of the K+ channel:

A 
4 individual alpha units (4 subunits)
6 transmembrane domains in each subunit
S4: positively charged voltage-sensing domain
S5-S6: pore forming domain (channel)
No Inactivation gate
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15
Q

Describe the states the Na+ channel can be in

A

Open (activated): cell permeable (voltage-dependent)
Activation gate: open
Inactivation gate: open

Inactivated: cell impermeable (time-dependent)
Activation gate: open
Inactivation gate: closed

Closed: cell permeable if big enough impulse
Activation gate: closed
Inactivation gate: open

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16
Q

Define Absolute Refractory Period (ARP)

Define Relative Refractory Period (RRP)

A

ARP: channels are the inactivated state
RRP: channels are in the closed state

17
Q

Describe how local anaesthetics work

A

Reversible block Na+ channels from within cells
Lipophilic, uncharged bases (B) diffuse across cell membrane
In the cells they become protonated (BH+) bind with Na+ channels inactivating them

18
Q

Describe the different pathways local anaesthetics can take

A

Hydrophobic pathway: aminoesters diffuse through membrane (not use-dependent)
Hydrophillic pathway: aminoamides diffuse from cytosol (use-dependent - only inactivate open channels)

(Aminoesters vs. Aminoamides: no. of ‘i’’s in the name)

19
Q

Define length constant

A

Distance for the action potential to decrease to 1/e of its original value

20
Q

Define capacitance

Define resistance

A

Capacitance: ability of the membrane to store charge
Resistance: difficulty of ion passing through the membrane (opposite of conductance)

21
Q

How do myelinated axons conduct action potentials so well?

A

Provides insulation from negative extracellular charges
High resistance: prevents leakage of ions (decreases conductance)
Low capacitance: prevents slowing of ions (increases length constant)

22
Q

What is saltatory conductance?

A

Node to node conductance of an action potential

23
Q

Describe saltatory conductance

A 
Action potential (Na+ influx) only appears at the nodes
Myelin insulates the cell membrane (decreases conductance)
The change in membrane potential is passed through the cytosol (local current flow)
24
Q

What effect does demyelination have on the axon and action potential?

A

Decreases resistance
Increases capacitance
Therefore the action potential may not reach the next node or be weaker than the threshold potential

25
Q

Describe the features of the Ca2+ channel

A

1 alpha unit (4 subunits linked together)
6 transmembrane domains in each subunit
S4: positively charged voltage-sensing domain
S5-S6: pore forming domain (channel)

26
Q

What is a neuromuscular junction

A

Where a nerve synapses with a skeletal muscle cell

ACh is released from the nerve cell and binds to a nAChR on the muscle cell

27
Q

Describe the process of neurotransmitter release from a nerve terminal

A

Action potential reaches nerve terminal
Depolarisation of the cell membrane opens voltage-gated Ca2+ channels (VGCC’s)
Ca2+ influx causes the release of vesicles of neurotransmitter
(Multiple AP’s, more Ca2+ influx and more vesicles released)

28
Q

How does the Ca2+ cause the release of neurotransmitter filled vesicles?

A

Ca2+ binds with synaptotagmin on the vesicles and helps dock with the snare complex
Complexin is removed from the snare complex forming a fusion core
Vehicle contents are exocytosed out of the function core

29
Q

What happens when ACh binds to the post-synaptic muscle cell?

A

2 ACh bind to nAChR to open the channel
Allows the exchange of Na+ and K+ producing an end-plate Potential
End-plate Potential depolarises the cell opening Na+ channels and creating an AP
AP causes the contraction of skeletal muscle fibre

30
Q

What are the types of antagonists of nAChR?

A

Competitive Inhibitors

Depolarising Inhibitors

31
Q

How do Competitive Inhibitors antagonise nAChR?

A

Bind to nAChR but do not cause depolarisation

Can be overcome by increasing the [ACh]

32
Q

How do Depolarising Inhibitors antagonise nAChR?

A

Bind to nAChR and cause maintained depolarisation
Inactivate Na+ channels
(Broken down by acetylcholinesterase)

33
Q

What are the disease states affecting conduction of the action potential (demyelinating)?

A

CNS -
Multiple Sclerosis
Devices disease (optic + spinal nerves)

PNS -
Landry-Guillain-Barre syndrome
Charcot-Marie-Tooth disease

34
Q

What is mayasthenia gravis?

A

Auto-immune disease targeting nAChR
Patients suffer muscle weakness (increases with exercise)
Antibodies target nAChR on the post synaptic membrane, destroying them (complement pathway)
The end-plate potential generated is reduced until no depolarisation occurs

ICPP (8 decks)

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