Nervous system signalling Flashcards

1
Q

Where do neurons receive input from other cells?

A

Dendrites

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2
Q

Which part of the neuron is involved in axon potential generation and transmission?

A

The axon

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3
Q

How do neurons pass information from themselves to another cell?

A

Via axon potential generation and transmission

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4
Q

What are the key features of a neuron?

A
  • axon hillock
  • myelin sheath
  • node of ranvier
  • synapse
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5
Q

What is a synapse?

A

Junction between 2 neurons

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6
Q

Where is the site of axon potential generation?

A

Axon hillock

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7
Q

What is a resting membrane potential?

A

more positive ions outside the cell and more negative ions inside the cell

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8
Q

Why is AP a negative value?

A

Measured in relation to outside

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9
Q

What is a typical RMP?

A

-60 to -70mV

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10
Q

How is RMP measured?

A

Electrophysiology

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11
Q

Which ions are key to the MP?

A
  • sodium
  • potassium
  • chloride
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12
Q

What is the distribution of ions in a negative MP?

A

Inside the cell is a low concentration of sodium and chloride
Outside the cell is a high concentration of sodium and chloride

Reverse is true for potassium

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13
Q

How do ions cross the membrane?

A

The membrane is not impermeable to ions

Has ion channels that allow passage of ions

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14
Q

What type of ion channels are usually present?

A
  • voltage gated (passive)
  • ligand gated (passive)
  • pumps (active)
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15
Q

What is the opening and closing of a voltage gated channel dependent on?

A
  • membrane potential

Different channels have different voltage dependencies

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16
Q

What is the opening and closing of a ligand gated channel dependent on?

A

Opened in response to binding

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17
Q

How does a pump allow the movement of ions across a membrane?

A

Usually requires energy in the form of ATP

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18
Q

What is the equilibrium potential?

A

Membrane potential where the number of ions entering a cell = the number of ions leaving a cell ( no net gain or loss)

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19
Q

Describe the movement of potassium from a negative membrane potential to equilibrium

A

High concentration of potassium inside the cell compared to outside
That makes potassium want to move down its concentration gradient to be outside the cell

This movement is counterbalanced by the electrical gradient

Potassium is a positively charged ion, whereas the cytoplasm of the cell is negatively charged
This makes potassium want to move down its electrical potential gradient into the cell

The overall equilibrium is based on the balance of these two gradients

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20
Q

What is the Nernst potential of sodium?

A

+ 66mV

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21
Q

What is the Nernst potential of potassium?

A
  • 88mV
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22
Q

What is the Nernst potential of chloride?

A

-62mV

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23
Q

What is an action potential?

A

A very brief but dramatic change in membrane potential

All or nothing response

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24
Q

What happens to a cell when it reaches action potential?

A

A cell will be sitting at resting membrane potential until something makes it less negative (depolarisation) making the cell reach its action potential threshold causing a sharp increase in membrane potential followed by a quick repolarisation. Small period where the cell becomes more negative than the resting membrane potential (hyperpolarisation) before reaching RMP.

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25
Q

Describe the shape of an AP on a graph

A

Similar to an ECG

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26
Q

What is related to depolarisation?

A

Increased permeability to Na+ ions

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27
Q

What causes repolarisation and hyperpolarisation?

A

Increased permeability to K+ ions

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28
Q

How does a cell reach its action potential?

A

Get a sudden opening of voltage-gated sodium channels, which causes a large influx of sodium into the cell

As sodium is positively charged the cell becomes less negative than it was before.

Technically overshoots and becomes more positive

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29
Q

What happens after the influx of sodium when a cell reaches its action potential?

A

Once the cell reaches a certain voltage, the voltage-gated ion channels will close, preventing any more sodium from entering the cell and the cell stops achieving membrane potential from the sodium

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30
Q

What happens so potassium during the closure of voltage gate sodium channels?

A

much slower opening of the potassium channels, allowing potassium to leave the cell.
This brings the membrane potential back down to RMP (repolarisation phase)
Also get hyperpolarisation phase, because a few more potassium channels leave the cell than necessary

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31
Q

How does the cell return to RMP after hyperpolarisation?

A

through the action of potassium-sodium pumps, which serves to achieve equilibrium

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32
Q

Which drugs manipulate the voltage gated sodium channel?

A
  • anaesthetics (lidocaine)
  • pain treatment
  • antiepileptic drugs
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33
Q

How does lidocaine work?

A

Lidocaine blocks voltage gated sodium channels meaning that sodium cannot enter the neuron, and therefore cannot fire action potentials and therefore cannot transmit information
Cannot feel pain for surgery

34
Q

What is the link between voltage-gated sodium channels and pain management?

A

Number of different subtypes of these voltage-gate sodium channels found in different areas of tissues.
A lot of interest currently in targeting the channels found on pain-sensing nerves, without causing the numbness that occurs with anaesthetics - ongoing research, nut currently available clinically

35
Q

How do antieplieptics work?

A

Epilepsy medication can work by blocking these channels to remove the hyperexcitability seen in this condition

36
Q

What does propagation mean?

A

how a signal travels down an axon to communicate with other cells

37
Q

How is propagation of the action potential achieved?

A

Does this through depolarisation.
The action potential is generated at the axon hillux, this patch of membrane is depolarised, which in turn depolarises the patch of membrane next to it.
This occurs down the axon, similar to a flow or depolarising wave

38
Q

Which direction does an AP travel?

A

The action potential only travels one way down the axon

Normally only generated at the axon hillux and travels down the axon but can occur the other way through electrical stimulation (not something that happens naturally)

39
Q

Where can a positive charge travel in a neuron?

A
  • Along the axon

- Out of the axon via membrane

40
Q

What does the destination of a current depend on?

A
  • Axon diameter (current will take the path of least resistance)
  • Number of open pores/channels in a membrane
41
Q

What factors facilitate faster conduction?

A
  • Wider diameters

- Insulation through myelin sheaths

42
Q

How does a myelin sheath facilitate faster conduction?

A

Through saltare conduction, allowing action potentials to jump between nodes of ranvier, reducing current leakage

43
Q

Which nerve fibers are myelinated?

A

A beta

A delta

44
Q

Which nerve fibers are unmyelinated?

A

C

45
Q

Which disorder is associated with defective myelination in the CNS?

A

Multiple sclerosis

46
Q

Which disorder is associated with defective myelination in the PNS?

A

Guillan-Barre syndrome

47
Q

How does MS occur?

A
  • Antibodies attack myelin
  • Formation of scars (sclerosis)
  • Delays /blocks action potentials
48
Q

What are the symptoms of MS?

A
  • Blurred vision
  • muscle pain
  • partial paralysis
  • fatigue
  • lack of coordination
49
Q

How does Guillan-Barre syndrome occur?

A
  • inflammatory disease
  • prior infection/inflammation
  • presence of inflammatory cells
50
Q

What are the symptoms of Guillan-Barre syndrome?

A
  • progressive motor weakness

- motor and sensory loss (face, limbs, trunk, diaphragm)

51
Q

What is synaptic transmission?

A

Chemical transmission between excitable cells

52
Q

What structures make up a synapse?

A
  • The presynaptic terminal
  • Postsynaptic membrane
  • synaptic vesicles
  • receptors
53
Q

What is the presynaptic terminal?

A

The terminal point of the axon of one neuron

54
Q

What is the postsynaptic membrane?

A

The dendrites or soma of another neuron

55
Q

What are the synaptic vesicles?

A

Vesciles within the presynaptic terminal that contain neurotransmitter

56
Q

What are the receptors in a synapse?

A

The receptors that a neurotransmitter will bind to that are found on the postsynaptic membrane

57
Q

What is an excitatory postsynaptic potential?

A

An EPSP brings the postsynaptic membrane closer to the threshold (depolarisation), therefore increasing the probability of the postsynaptic cell producing an action potential

58
Q

When does an EPSP occur?

A

When a positive ion enters the cell through synaptic transmission

59
Q

What is different between an AP and an EPSP?

A
AP = all or nothing
EPSP = vary in sizes
60
Q

What is an inhibitory postsynaptic potential?

A

An IPSP moves the post-synaptic membrane further away from the threshold (hyperpolarisation), therefore reducing the probability of the postsynaptic cell producing an action potential

61
Q

When does an IPSP occur?

A

When a negative ion enters the cell from synaptic transmission

62
Q

What is temporal summation?

A

If two APs arrive in close succession, the first one may depolarise the cell halfway but not enough to trigger an AP, but the second one arrives quickly after and that further depolarises the cell, which reaches the threshold to trigger an AP.

63
Q

What is spatial summation?

A

Is similar to temporal summation, but rather than a couple of APs arrive in close succession from one axon, we can get multiple APs arriving from multiple axons to the same cell

These processes can also occur with inhibitory postsynaptic potentials (IPSP), however these will not drive action potentials, these will just further inhibit the cell from reaching threshold

64
Q

What are the main types of neurotransmitters?

A
  • Cholinergic
  • Biogenic amines
  • Amino acids
  • Neuropeptides
  • Other
65
Q

Name a cholinergic neurotransmitter

A

Acetylcholine

66
Q

Name different biogenic amine neurotransmitters

A
  • Catecholamines: noradrenaline, adrenaline, dopamine

- 5-hydroxytryptamine: 5-HT/serotonin

67
Q

Name different amino acid neurotransmitters

A
  • Excitatory: glutamate

- Inhibitory: gamma-aminobutyric acid (GABA)

68
Q

Name a neuroeptide neurotransmitter

A

endogenous opiods

69
Q

Name other examples of neurotransmitters

A
  • gases: nitric oxide

- pruines: adenosine, ATP

70
Q

Name two disorders caused by disruption of synaptic transmission

A
  • Botulism
  • Myasthenia gravis

Both affect the neuromuscular junction

71
Q

How does botulism occur?

A
  • clostridium bacteria produce botulinum toxin (contaminated food)
  • disrupts exocytosis, preventing ACh release
72
Q

What are the symptoms of botulism?

A
  • skeletal muscle weakness

- paralysis of the diaphragm (respiratory failure)

73
Q

How does myasthenia gravis occur?

A
  • inflammatory disease

- antibodies bind to ACh receptors in the postsynaptic membrane at the motor end plate

74
Q

What are the symptoms of myasthenia gravis?

A
  • severe muscle weakness

- particularly affects; eyelids, eyes, face, throat and limb muscles

75
Q

What are the different routes of spreading information in the nervous system?

A
  • Divergence (one neuron can pass information to many neurons)
  • Convergence (many neurons pass information to one neuron, which integrates the information)
76
Q

How is cortical representation of sensory and motor shown?

A

Via the homunculus

77
Q

What ways can cerebral function be investigated?

A
  • EEG
  • PET
  • fMRI
  • TMS
78
Q

How does an EEG work and what is its uses?

A

(electro-encephalography)
- records the electrical activity of the brain

used to investigate the cognitive processes in response to a stimulus

79
Q

How does an PET work and what is its uses?

A

(positron emission tomography)
Measures blood flow, via a small dose of radioactive material injected into the bloodstream

Able to locate brain activity while performing a task

80
Q

How does an fMRI work and what is its uses?

A

(functional magnetic resonance imaging)
Measures blood flow

Able to locate brain activity while performing a task

81
Q

How does an TMS work and what is its uses?

A

(Transcranial magnetic stimulation)

uses electromagnet to stimulate brain activity, causing depolarisation or interrupted firing

Able to interrupt brain activity while performing a task