Synaptic Transmission Flashcards

1
Q

What is a synapse?

A

A synapse is the junction between a neurone and another neurone, or between a neurone and an effector cell.

e.g. a muscle or gland cell.

Gap = synaptic cleft

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2
Q

What do you need to remember about the presynaptic neurone?

A

It has a swelling called a synaptic knob.

This contains synaptic vesicles filled with chemicals called neurotransmitters.

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3
Q

Outline how an A.P crosses the synapse.

A

At the end of a neurone an A.P causes neurotransmitters to be released into the synaptic cleft. They diffuse across to the postsynaptic membrane (the one after the synapse) and bind to specific receptors.

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4
Q

Describe what happens after a chemical message has diffused across the synapse.

A

When neurotransmitters bind to receptors they might trigger an action potential (in a neurone), cause muscle contraction (in a muscle cell), or cause a hormone to be secreted (from a gland cell).

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5
Q

What makes impulses unidirectional?

A

Unidirectional - only travel in one direction.

Synaptic vesicles only in the presynaptic neurone.

The receptors are only on the postsynaptic membrane.

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6
Q

How is the response stopped after enough chemicals have diffused across the synapse?

A

Neurotransmitters are removed from the cleft so the response doesn’t keep happening, e.g. they’re taken back
into the presynaptic neurone or they’re broken down by enzymes (and the products are taken into the neurone).

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7
Q

Typical structure of a synapse.

A
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8
Q

E.g.s of neurotransmitters

A

Acetylcholine

Noradrenaline

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9
Q

How is a nerve impulse transmitted across a Cholinergic synapse?

A

ACh Transmits the Nerve Impulse Across a Cholinergic Synapse

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10
Q

What does it mean if a neurotransmitter is excitatory?

A

Excitatory neurotransmitters depolarise the postsynaptic membrane, making it fire an action potential if the threshold is reached.

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11
Q

At what synapses does ACh have an excitatory effect? Explain.

A

acetylcholine is an excitatory neurotransmitter at (cholinergic) synapses in the CNS.
- it binds to (cholinergic) receptors to cause an action potential in the postsynaptic membrane

  • and at neuromuscular junctions.
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12
Q

What does it mean if a neurone is inhibitory?

A

Inhibitory neurotransmitters hyperpolarise the postsynaptic membrane (make the potential difference more negative), preventing it from firing an action potential.

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13
Q

At what synapses does ACh have an inhibitory effect? Explain.

A

E.g. acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart. When it binds to receptors here, it can cause potassium ion channels to open on the postsynaptic membrane, hyperpolarising it. (so k+ ions move out).

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14
Q

What is summation?

A

If a stimulus is weak, only a small amount of neurotransmitter will be released from a neurone into the synaptic cleft.

This might not be enough to excite the postsynaptic membrane to the threshold level and stimulate an action potential.

Summation is where the effect of neurotransmitter released from many neurones (or one neurone that’s stimulated a lot in a short period of time) is added together.

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15
Q

What are the two types of summation?

A
  1. Spatial summation
  2. Temporal summation
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16
Q

Describe spatial summation.

A
17
Q

Describe temporal summation.

A
18
Q

What are neuromuscular junctions?

A

The synapse between a motor neurone and a muscle cell.

19
Q

Which neurotransmitter is used at neuromuscular junctions and how?

A

Neuromuscular junctions use the neurotransmitter acetylcholine (ACh), which binds to cholinergic receptors called nicotinic cholinergic receptors.

20
Q

Neuromuscular junctions work in basically the same way as the cholinergic synapse.

Describe how neuromuscular junctions work.

A
  • The postsynaptic membrane has lots of folds that form clefts. These clefts store the enzyme that breaks down ACh (acetylcholinesterase - AChE).

-The postsynaptic membrane has more receptors than other synapses.

  • ACh is always excitatory at a neuromuscular junction. So when a motor neurone fires an action potential, it normally triggers a response in a muscle cell. This isn’t always the case for a synapse between two neurones.
21
Q

Outline 5 different ways drugs can affect synaptic transmission.

A
  1. Agonists
  2. Antagonists
  3. Inhibit the enzyme
  4. Stimulate the release of neurotransmitter from the presynaptic neurone.
  5. Inhibit the release of neurotransmitter from the presynaptic neurone.
22
Q

Describe the effects of agonists on synaptic transmission.

A

Agonists - same shape as neurotransmitters so they mimic their action at receptors.
This means more receptors are activated.

E.g. nicotine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain.

23
Q

Describe the effect of antagonists on synaptic transmission.

A

Antagonists - blocks receptors so they can’t be activated by neurotransmitters. This means fewer receptors (if any) can be activated.

E.g. curare blocks the effects of acetylcholine by blocking nicotinic cholinergic receptors at neuromuscular junctions, so muscle cells can’t be stimulated. This results in the muscle being paralysed.

24
Q

Describe the effect of drugs that inhibit enzymes on synaptic transmission.

A

Some drugs inhibit the enzyme that breaks down neurotransmitters.

This means there are more neurotransmitters in the synaptic cleft to bind to receptors and they’re there for longer.

E.g. nerve gases stop acetylcholine from being broken down in the synaptic cleft. This can lead to loss of muscle control.

25
Q

Describe the effect of drugs that stimulate the release of neurotransmitters on synaptic transmission.

A

Some drugs stimulate the release of neurotransmitter from the presynaptic neurone so more receptors are activated, e.g. amphetamines.

26
Q

Describe the effect of drugs that inhibit the release of neurotransmitters on synaptic transmission.

A

Some drugs inhibit the release of neurotransmitters from the presynaptic neurone so fewer receptors are activated, e.g. alcohol.

27
Q

Q1. The graph on the right shows the potential difference across a postsynaptic membrane against time.

a) Suggest why a potential difference of -45 mV is significant for this postsynaptic membrane.

b) The action potential shown on the graph was fired as a result of temporal summation.

Use the graph and your own knowledge to explain how this action potential was created.

A

1 a) It is the threshold that needs to be reached for an action potential to fire.

b)
- before the action potential fired, the potential difference across the membrane increased three times in quick succession.

  • The increases in potential difference were caused by nerve impulses arriving at the synapse and releasing neurotransmitter, which caused sodium ion channels to open on the postsynaptic membrane.
  • This allowed an influx of sodium ions into the postsynaptic membrane, which increased the potential difference across the membrane.
    It was not until the arrival of the third impulse that enough neurotransmitter was acting on the membrane to allow the threshold level to be reached and the action potential to be fired.
28
Q

Q2. Myasthenia gravis is a disease in which the body’s immune system gradually destroys receptors at neuromuscular junctions. This leads to weaker muscular responses than normal. Explain why.

A
  1. There will be fewer receptors for acetylcholine/ACh to bind to, so fewer sodium ion channels will open at neuromuscular junctions, making it less likely that action potentials will be generated in the muscle cells.
29
Q

Q3. Galantamine is a drug that inhibits the enzyme acetylcholinesterase (AChE). Predict the effect of galantamine at a neuromuscular junction and explain your answer.

A

3 Galantamine would stop acetylcholinesterase/AChE breaking down acetylcholine/ACh, so there would be more acetylcholine/ ACh in the synaptic cleft and it would be there for longer.
This means more nicotinic cholinergic receptors would be stimulated.