nervous coordination flashcards

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30 Terms

1
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What initial event occurs at the synaptic knob of the presynaptic neurone?

An action potential arrives at the synaptic knob of the presynaptic neurone.

2
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What does the action potential stimulate in the presynaptic neurone?

The action potential stimulates voltage-gated calcium ion channels in the presynaptic neurone to open.

3
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What happens after the calcium ion channels open?

Calcium ions diffuse into the synaptic knob. They are pumped out afterwards by active transport.

4
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What is the effect of the influx of calcium ions into the synaptic knob?

The influx of calcium ions causes the synaptic vesicles to move to and fuse with the presynaptic membrane.

5
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What neurotransmitter is released into the synaptic cleft, and what is this process called?

The vesicles release the neurotransmitter acetylcholine (ACh) into the synaptic cleft. This process is called exocytosis.

6
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What happens to ACh after it diffuses across the synaptic cleft?

ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the postsynaptic membrane.

7
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What occurs on the postsynaptic membrane when ACh binds to its receptors?

The influx of sodium ions into the postsynaptic membrane causes depolarisation. An action potential on the postsynaptic membrane is generated if the threshold is reached.

8
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How is ACh removed from the synaptic cleft, and why is this important?

ACh is removed from the synaptic cleft by the enzyme acetylcholinesterase (AChE) to prevent continuous response. The products are re-absorbed by the presynaptic neurone and used to make more ACh.

9
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Describe the additional features of a myelinated motor neuron.

  • Schwann cells: wrap around axon many times.

  • Myelin sheath: made from myelin-rich membranes of
    Schwann cells.

  • Nodes of Ranvier: very short gaps between neighbouring Schwann cells where there is no myelin sheath.

10
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Name 3 processes Schwann cells are involved in.

  • electrical insulation

  • phagocytosis

  • nerve regeneration

11
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Explain why myelinated axons conduct impulses faster than unmyelinated axons

Saltatory conduction: Impulse 'jumps' from one node of Ranvier to another. Depolarisation cannot occur where myelin sheath acts as electrical insulator.

So impulse does not travel along whole axon length.

12
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What is resting potential?

Potential difference (voltage) across neuron membrane when not stimulated (-50 to -90 mV, usually about -70 mV in humans).

13
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How is resting potential established?

• The resting potential is maintained by a sodium-potassium pump, involving active transport and therefore ATP.

• The pump moves 2 Ktions in and 3 Nat ions out.

• This creates a electrochemical gradient and results in K+ diffusing out and Nat diffusing in, however because the membrane is more permeable to K+ more are moved out resulting in the -70mV.

14
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Name the stages in generating an action potential.

  1. Depolarisation

  2. Repolarisation

  3. Hyperpolarisation

  4. Return to resting potential

15
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What happens during depolarisation?

  1. Stimulus→facilitated diffusion of Nations into cell down electrochemical gradient.

  2. p.d. across membrane becomes more positive.

  3. If membrane reaches threshold potential (-50mV), voltage-gated Nat channels open.

  4. Significant influx of Nations reverses p.d. to
    +40mV.

16
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What happens during repolarisation?

  1. Voltage-gated Na* channels close and voltage-gated K* channels open.

  2. Facilitated diffusion of K* ions out of cell down their electrochemical gradient.

  3. p.d. across membrane becomes more negative.

17
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In the nerve pathway explain how, synapses ensure that the nerve impulses travel towards the muscle fibre

  • neurotransmitter is only made / stored in pre - synaptic neurone

  • Neuroreceptors only on the post synaptic membrane

18
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Axon P was found to conduct impulses much faster than other axons in the nerve pathwaY. Describe and explain one feature of axon P that might cause this difference.

  • axon P is myelinated

  • So shows saltatory conduction / impulses jump nodes of Ranvier

Or

  • Axon p has a larger diamter

  • So less resistance to flow of ions

19
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20
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What is the purpose of summation at a synapse?

Summation allows for the integration of multiple stimuli, enabling a finely tuned nervous response even from individually weak signals that might not independently reach the postsynaptic membrane's threshold for an action potential.

21
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Explain the general concept of summation at a synapse.

Summation is the process by which a postsynaptic neuron integrates the effects of multiple excitatory and/or inhibitory neurotransmitter signals from one or more presynaptic neurons, determining whether an action potential is triggered.

22
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Describe spatial summation.

Spatial summation occurs when multiple presynaptic neurons simultaneously release neurotransmitters onto a single postsynaptic neuron. The combined effect of these simultaneous inputs can collectively reach the threshold, triggering an action potential.

23
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What happens in spatial summation if some presynaptic neurons release inhibitory neurotransmitters?

In spatial summation, if some presynaptic neurons release an inhibitory neurotransmitter, their hyperpolarizing effect can counteract the excitatory neurotransmitters, preventing the postsynaptic neuron from reaching the threshold and thus inhibiting an action potential.

24
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Describe temporal summation.

Temporal summation occurs when a single presynaptic neuron fires multiple times in quick succession, releasing neurotransmitter repeatedly. This rapid accumulation of neurotransmitter in the synaptic cleft makes it more likely for the postsynaptic neuron to reach its threshold and generate an action potential.

25
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How do agonist drugs affect synaptic transmission? Provide an example.

Agonist drugs mimic the action of natural neurotransmitters by having a similar molecular shape, allowing them to bind to and activate specific receptors. This binding leads to an increased activation of postsynaptic receptors. For example, nicotine acts as an agonist for acetylcholine at nicotinic cholinergic receptors in the brain.

26
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How do antagonist drugs affect synaptic transmission? Provide an example.

Antagonist drugs block specific neurotransmitter receptors, preventing the natural neurotransmitter from binding and activating them. This reduces or eliminates the activation of these receptors. For instance, curare blocks acetylcholine receptors at neuromuscular junctions, leading to muscle paralysis.

27
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How do drugs that inhibit enzyme breakdown of neurotransmitters affect synaptic transmission? Provide an example.

These drugs inhibit the activity of enzymes responsible for breaking down neurotransmitters within the synaptic cleft. By preventing enzymatic degradation, they prolong the presence and action of neurotransmitters on postsynaptic receptors. Nerve gases, for example, inhibit acetylcholinesterase, causing prolonged acetylcholine activity and loss of muscle control.

28
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How do some drugs stimulate the release of neurotransmitters from the presynaptic neuron? Provide an example.

Some drugs increase the exocytosis of neurotransmitters from the presynaptic neuron into the synaptic cleft. This leads to a higher concentration of neurotransmitters available to bind with postsynaptic receptors, increasing receptor activation. Amphetamines are an example of drugs that stimulate neurotransmitter release.

29
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How do some drugs inhibit the release of neurotransmitters from the presynaptic neuron?

Some drugs reduce or prevent the release of neurotransmitters from the presynaptic neuron into the synaptic cleft. This results in fewer neurotransmitters binding to postsynaptic receptors, thereby decreasing receptor activation and the likelihood of an action potential.

30
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Describe and explain how the membrane potential changes during depolarisation (4 marks)

• A stimuli causes more sodium ion channels in the membrane to open so the membrane becomes more permeable to sodium ions

• As a result the sodium ions move into the axon through open channels via facillitated diffusion

• This results in an imbalance of positive ions, with more ions inside the axon than outside

• The resulting membrane potential is positive, reaching a peak of about +40mV