Physiology - Nerve & Muscle Cells Flashcards

1
Q

Define resting membrane potential

A
  • describes the difference in charge across a cell membrane at rest as a result of separation of positive and negative charges
  • requires a concentration gradient with different membrane permeabilities and unequal distribution of ions (mainly Na+/K+)
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2
Q

How is resting membrane potential created?

A
  • Na+K+ATPase maintains the gradient by pumping 3 Na+ out for 2 K+ in
  • Na+ and K+ then move down their concentration gradient (Na+ moves in, K+ moves out)
  • at rest there are more open K+ channels than Na+ channels, thus permeability of K+ is greater and net movement of K+ out
  • K+ concentration gradient is the main determinant of the resting membrane potential
  • inside of cell is negative relative to outside
  • RMP neuron = -70, RMP muscle cell = -90
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3
Q

Why is a cell more excitable in hyperkalaemia

A

RMP moves closer to threshold potential for eliciting an action potential

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4
Q

Describe the sequence of events in skeletal muscle contraction/relaxation

A

1) resting membrane potential in skeletal muscle is -90mV
2) build up of EPSP, not a full action potential yet
- ligand-gated Na+ channels are open and Na+ moving into the cell, moving towards the threshold potential of -55mV
3) threshold potential is reached and voltage-gated Na+ channels open with rapid influx of Na+ into the cell (depolarisation)
- action potential spreads along T tubules, activating voltage-gated DHPR
- DHPR interacts with RYR on SR, causing release of calcium from the SR
- calcium binds to troponin C, causing a shift in tropomyosin to uncover myosin binding site on actin
- myosin now able to interact with actin, forming cross bridge and the power stroke
4) membrane potential moves towards equilibrium potential for Na+, causing closure of Na+ channels at around +20
5) voltage-gated K+ channels open, causing K+ to move out of cell and fall in membrane potential (repolarisation)
- calcium is pumped back into SR and released from tropomyosin, thus ending interaction between actin and myosin
6) slow return of K+ channels to resting state (after hyper-polarisation)
7) return to resting potential

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5
Q

Draw a skeletal muscle action potential

A
  • initial action potential travels down axon and causes opening of voltage-gated calcium channels
  • this causes release of NT acetylcholine from pre-synaptic vesicles
  • ACh binds to nicotinic post-synaptic membrane receptors, increases Na+ conductance, causing an EPSP
  • once threshold level is reach, there is an action potential
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6
Q

Describe summation of contraction

A
  • summation of contraction occurs when there is repeated stimulus before relaxation occurs
  • the contractile mechanism itself does not have a refractory period, so there is repeated contractile response
  • with rapidly repeated stimulation, individual responses fuse into one continuous contraction = tetanic contraction
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7
Q

In the synapse, where can inhibition occur

A
  • pre-synaptic: occurs on axon to axon synapses, causes reduction in Ca+2 conductance and thus NT release
  • post-synaptic: occurs by GABA causing increased Cl- conductance, altering RMP so less likely to fire
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8
Q

What are the major different types of skeletal muscle

A
  • type 1 = slow, oxidative, red colour, small diameter SO
  • type 2 = fast, glycolytic, white colour, large diameter FG
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9
Q

Describe the contraction of visceral smooth muscle

A
  • starts with binding of acetylcholine to muscarinic receptors
  • causes increased Ca+2 influx into cell from extracellular fluid and not SR
  • calcium binds to calmodulin, activating the calmodulin-dependent myosin light chain kinase
  • phosphorylation of myosin -> binding to actin and contraction
  • dephosphorylation of myosin light chain by phosphatase -> relaxation of muscle
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10
Q

What influences intestinal smooth muscle contraction

A
  • increased by: cold, stretch, ACh, phospholipase C
  • decreased by: sympathetic stimulation, cAMP
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11
Q

Where are ion channels distributed in myelinated neurons

A

voltage-gated Na+ channels are concentrated at Nodes of Ranvier

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12
Q

What affects conduction

A

myelinated vs demyelinated
saltatory vs non-saltatory
diameter
direction of conduction

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13
Q

What are the classes of nerve fibers

A
  • A alpha: somatic motor and proprioception
  • B beta: touch and pressure
  • A gamma: motor to muscle spindle
  • A delta: pain and temperature
  • B: preganglionic autonomic
  • C dorsal roots: pain and temperature
  • C sympathetic: postganglionic
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14
Q

What is the relevance of fibre types to emergency medicine

A

small diameter pain fibres are more susceptible to local anaesthetic than motor

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15
Q

Draw and describe the action potential of a neuron

A

1) resting membrane potential of -70mV, action potential on pre-synaptic membrane causes release of ACh
ACh binds to post-synaptic nicotinic receptors, opening ligand-gated Na+ channels
2) ligand-gated Na+ channels are open and Na+ moving into the cell, moving towards the threshold potential of -55mV
3) threshold potential is reached and voltage-gated Na+ channels open with rapid influx of Na+ into the cell (depolarisation)
4) membrane potential moves towards equilibrium potential for Na+ → Na+ channels close
5) voltage-gated K+ channels open → K+ moves out of cell → repolarisation
6) slow return of K+ channels to closed state = after-hyper-polarisation
7) return to resting potential

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