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

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
What are the nodes of Ranvier?
Short intervals of axon not covered in myelin sheath where Na+ channels are concentrated.
26
Function of nodes of Ranvier
Allows for saltatory conduction which increases conduction velocity of axons, and allows waste/nutrients to exit/enter.
27
What is saltatory conduction?
When the AP jumps from node to node.
28
Where do chemical synapses occur?
Between neurons and: other neurons, muscle cells, gland cells
29
Name of the gap between presynaptic and postsynaptic cell
synaptic cleft
30
Chain of events at a chemical synapse
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
What can neurotransmitters be made of?
Amino acid derivatives (e.g. ACh, dopamine, GABA, glutamate), peptides (VIP, endorphins)
32
Examples of amino acid derived Tx
ACh, dopamine, GABA, glutamate, glycine, noradrenaline, serotonin
33
Examples of neurotransmitters derived from peptides
substance P, VIP (vasoactive intestinal polypeptide), enkephalins, endorphins
34
How can the same neurotransmitter have a different effect on post-synaptic cells?
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
What is an exhibitory synapse?
Tx causes depolarisation of the postsynaptic cell, bringing the MP closer to threshold for AP firing (exhibitory postsynaptic potential, EPSP)
36
What is an inhibitory synapse?
Neurotransmitter causes hyperpolarisation which takes MP further away from firing threshold (inhibitory postsynaptic potential, IPSP)
37
Where on a neuron can inputs synapse?
On dendrites and cell body.
38
What is summation?
When excitatory postsynaptic potentials (EPSP) are added together to drive the MP beyond threshold.
39
How does summation occur?
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
Term given when a neuron receives many inputs from other cells
Convergence
41
Term given when a neuron synapses with many other cells
divergence
42
What will usually happen when EPSPs and IPSPs summate?
Cancel each other out
43
How do neurons act as processors?
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
Name of synapse between motor nerve and muscle fibre
neuromuscular junction / motor end plate
45
How does the area of contact in a neuromuscular junction compare to a nerve-nerve synapse?
Area of contact in neuromuscular junction is greater
46
What is the neurotransmitter released at a neuromuscular junction?
Acetylcholine
47
Which enzyme breaks down ACh?
Acetylcholinesterase - nerve reuptakes choline and acetate
48
Sequence of events at a neuromuscular junction
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
How can drugs enhance / supress synaptic activity?
By affecting the synthesis/storage of Tx, release of Tx, action of Tx on receptor, second messenger, inactivating Tx
50
How does Botox (botulinum toxin) paralyse facial muscles?
By preventing the release of ACh from motor nerve endings.