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BDS1 > Nervous conduction and transmission > Flashcards

Nervous conduction and transmission Flashcards

1
Q

What is the resting membrane potential?

A

A potential difference across the membrane of negative 20-90mV (approx -70mV). The membrane is ‘polarised’

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2
Q

At resting membrane potential, which side of the membrane is more negative?

A

Inside (ICF) is more negative than the outside (ECF)

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3
Q

How is the membrane polarised despite there being equal numbers of positive and negative charges on each side of the membrane?

A

Charges are unevenly distributed - all negative just inside the membrane, all positive just outside the membrane.

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4
Q

Significance of different concentrations of ions in ICF and ECF

A

e.g. much greater Na+ conc in ECF, greater K+ in ICF. Indicates presence of Na+/K+ pump.

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5
Q

During resting membrane potential, which channels are open/closed?

A

Some K+ channels are open. Na+ channels are closed.

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6
Q

How does the resting membrane potential arise?

A

The Na+/K+ pump moves 3 Na+ out and 2 K+ in. K+ is able to diffuse out of cell via open K+ channels down the concentration gradient. This creates a more positive cell exterior than interior.

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7
Q

How can the membrane potential be altered?

A

By applying an electrical current to the cell (a stimulus)

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8
Q

In which direction does a hyperpolarising current move the membrane potential?

A

Further away from 0 (more negative)

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9
Q

In which direction does a depolarising current move the membrane potential?

A

Closer to 0 (more positive)

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10
Q

Why are depolarisation and hyperpolarisation considered to be ‘graded’ responses?

A

The amplitude depends on the size of the stimulus (until threshold is reached)

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11
Q

When will an action potential occur?

A

When the depolarisation reaches the threshold (approx -55mV) this causes voltage-gated Na+ channels to open. Influx of Na+ causes the MP to reach about +35mV.

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12
Q

Why is an action potential considered to be an ‘all or nothing’ event?

A

If the threshold is reached, the amplitude of the AP is independent of the stimulus intensity.

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13
Q

What happens once the MP reaches +35mV in an action potential?

A

Voltage-gated Na+ channels shut, voltage-gated K+ channels open. K+ diffuse out of the cell which leads to repolarisation (MP becomes more negative).

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14
Q

Why does hyperpolarisation occur?

A

Due to a small K+ overshoot.

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15
Q

Stages of an action potential

A

A stimulus causes depolarisation that reaches the threshold (-55mV) resulting in Na+ channels opening and Na+ diffusing in creating further depolarisation. At +35mV, Na+ channels close and K+ channels open causing K+ diffuse out resulting in repolarisation. A K+ overshoot causes hyperpolarisation. Resting potential is then restored.

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16
Q

How do local anaesthetics work?

A

Stop nerve conduction by binding to an internal site on Na+ channels which blocks them.

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17
Q

What is the refractory period?

A

Period of in excitability after an AP has been initiated. Due to inactivation of voltage-gated Na+ channels

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18
Q

Advantage of having a refractory period

A

AP are unidirectional - previous Na+ channels are inactivated

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19
Q

How are APs propagated?

A

As waves of depolarisation. The current flows in ICF and ECF from positive to negative regions which alters the membrane potential in adjacent regions.

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20
Q

Effect of axon diameter on propagation speed

A

Speed of AP propagation increases with axon diameter

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21
Q

Why do squid giant axons relate to propagation in human axons?

A

Squids’ giant axons are up to 1mm in diameter with a conduction velocity of 35m/s. The axons are too large and conduction too slow for vertebrates so a way of increasing conduction speed while decreasing diameter evolved (myelination)

22
Q

Maximum speed of conduction in a myelinated neuron

A

120 m/s

23
Q

How are axons myelinated?

A

Axons are gradually wrapped in concentric layers of Schwann/glial plasma membrane (neurilemma).

24
Q

Function of myelination

A

Insulates the axon and improves conduction speed.

25
Q

What are the nodes of Ranvier?

A

Short intervals of axon not covered in myelin sheath where Na+ channels are concentrated.

26
Q

Function of nodes of Ranvier

A

Allows for saltatory conduction which increases conduction velocity of axons, and allows waste/nutrients to exit/enter.

27
Q

What is saltatory conduction?

A

When the AP jumps from node to node.

28
Q

Where do chemical synapses occur?

A

Between neurons and: other neurons, muscle cells, gland cells

29
Q

Name of the gap between presynaptic and postsynaptic cell

A

synaptic cleft

30
Q

Chain of events at a chemical synapse

A
  1. AP arrives in the presynaptic neuron
  2. Depolarisation causes voltage-gated Ca2+ channels to open resulting in an influx of Ca2+.
  3. Causes vesicles containing neurotransmitter (Tx) to move towards and fuse with the presynaptic membrane.
  4. Tx released by exocytosis and diffuses across synaptic cleft.
  5. Tx binds to ligand-gated Na+ channels on the postsynaptic membrane causing them to open.
  6. Change occurs in postsynaptic cell
  7. Tx is inactivated by enzymic destruction and reuptake into presynaptic cell.
31
Q

What can neurotransmitters be made of?

A

Amino acid derivatives (e.g. ACh, dopamine, GABA, glutamate), peptides (VIP, endorphins)

32
Q

Examples of amino acid derived Tx

A

ACh, dopamine, GABA, glutamate, glycine, noradrenaline, serotonin

33
Q

Examples of neurotransmitters derived from peptides

A

substance P, VIP (vasoactive intestinal polypeptide), enkephalins, endorphins

34
Q

How can the same neurotransmitter have a different effect on post-synaptic cells?

A

A different type of receptor on the postsynaptic membrane and different secondary messenger can lead to a different effect. e.g. exhibitory and inhibitory synapses

35
Q

What is an exhibitory synapse?

A

Tx causes depolarisation of the postsynaptic cell, bringing the MP closer to threshold for AP firing (exhibitory postsynaptic potential, EPSP)

36
Q

What is an inhibitory synapse?

A

Neurotransmitter causes hyperpolarisation which takes MP further away from firing threshold (inhibitory postsynaptic potential, IPSP)

37
Q

Where on a neuron can inputs synapse?

A

On dendrites and cell body.

38
Q

What is summation?

A

When excitatory postsynaptic potentials (EPSP) are added together to drive the MP beyond threshold.

39
Q

How does summation occur?

A

Many excitatory inputs are received by a neuron within a short time period (either from multiple neurons (spatial summation) or the same neuron (temporal summation)).

40
Q

Term given when a neuron receives many inputs from other cells

A

Convergence

41
Q

Term given when a neuron synapses with many other cells

A

divergence

42
Q

What will usually happen when EPSPs and IPSPs summate?

A

Cancel each other out

43
Q

How do neurons act as processors?

A

They receive and integrate many inputs some of which are excitatory and inhibitory. Neuron is more likely to fire if the excitatory input predominates.

44
Q

Name of synapse between motor nerve and muscle fibre

A

neuromuscular junction / motor end plate

45
Q

How does the area of contact in a neuromuscular junction compare to a nerve-nerve synapse?

A

Area of contact in neuromuscular junction is greater

46
Q

What is the neurotransmitter released at a neuromuscular junction?

A

Acetylcholine

47
Q

Which enzyme breaks down ACh?

A

Acetylcholinesterase - nerve reuptakes choline and acetate

48
Q

Sequence of events at a neuromuscular junction

A
  1. AP depolarises motor nerve ending which opens Ca2+ channels
  2. Influx of Ca2+ results in vesicles migrating towards and fusing with the presynaptic membrane.
  3. ACh released by exocytosis into synaptic cleft
  4. ACh diffuses across cleft and binds to Na+ receptors on the postsynaptic cell
  5. AP in muscle cell causes contraction
  6. ACh broken down by AChase
  7. Choline and acetyl uptaken by neuron
49
Q

How can drugs enhance / supress synaptic activity?

A

By affecting the synthesis/storage of Tx, release of Tx, action of Tx on receptor, second messenger, inactivating Tx

50
Q

How does Botox (botulinum toxin) paralyse facial muscles?

A

By preventing the release of ACh from motor nerve endings.

BDS1 (50 decks)

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