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PHAY0003 > Nerves and Neurotransmitters > Flashcards

Nerves and Neurotransmitters Flashcards

1
Q

What are nerves?

A

A bundle of fibres that transmit impulses from various parts of the body to the brain or spinal cord and back

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2
Q

What are the 2 nervous systems in the body called?

A

Central nervous system

Peripheral nervous system

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3
Q

What does it mean to be linked anatomically and functionally?

A

Connect physically and through impulses

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4
Q

What are the 2 systems within the PNS?

A

Afferent (sensory) and efferent (motor)

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5
Q

What does the afferent system do?

A

It transmits information about senses from sensory organs to other parts of the body

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6
Q

What are the 2 systems within the efferent system?

A

Somatic and autonomic system

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7
Q

What does the somatic system control?

A

Contraction of skeletal muscle (voluntary)

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8
Q

What does the autonomic system control?

A

Regulating the involuntary activity of organs such as heart, GI tract, blood vessels and certain glands

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9
Q

What are the 2 systems within the autonomic nervous system?

A

Sympathetic and parasympathetic

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10
Q

What is the enteric nervous system?

A

Part of the PNS (autonomic) which is entirely within the GI tract

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11
Q

What are the 2 types of cells in the nervous system?

A

Neurons and glia

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12
Q

What is the names for the glia cells in the CNS?

A

Astrocytes and oligodendrocytes

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13
Q

What is the names for the glia cells in the PNS?

A

Schwann cells

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14
Q

What are Schwann cells and oligodendrocytes important for?

A

The conduction of nerve impulses known as action potentials

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15
Q

What are action potentials?

A

Nerve impulses

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16
Q

What is the soma?

A

The cell body of neurons

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17
Q

What is the axon?

A

Fibres that leave the soma from the axon hillock which then travels to its target muscle or neuron.

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18
Q

What is the axon terminal?

A

The ends of axons which makes a synaptic connection with its target

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19
Q

Describe mammalian axons

A

They are narrow and are relatively short in the CNS compared to when in the PNS. In the PNS they tend to form nerve trunks

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20
Q

What is a nerve trunk?

A

A bundle of nerve fibres enclosed in a connective tissue sheath

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21
Q

What are dendrites?

A

Points of contact for axons from other neurons

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22
Q

What are neurotransmitters?

A

Chemical signal molecules released from neurons

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23
Q

How are neurotransmitters transferred between neurons

A

After being released from a neuron, they bind to receptors on dendrites and form a drug-receptor complex which triggers signals within neurons. The signals are transferred to the soma.

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24
Q

Describe the differences in ion concentration inside and outside of a neuron for Na+, K+ and Ca+

A 
Na+ = low inside the cell
K+ = high inside the cell
Ca+ = low inside the cell
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25
Q

What in neuron membranes allows the ionic concentrations to be maintained?

A

Pumps and ion channels

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26
Q

Describe what the Na+/K+ ATPase pump does

A

Binds a molecule of ATP with 3 NA+ ions inside the neuron causing the ATP to be hydrolysed leading to the pump being phosphorylated and a change in conformation. The 3 NA+ are released outside and the 2 K+ binding sites are then exposed and bound to. This dephosphorylates the pump so that it reverts to its original conformation, transporting the K+ ions inside the neuron

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27
Q

When are leak K+ channels open on neurons?

A

At rest

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28
Q

Why is a membrane potential generated on neurons?

A

There is a difference in concentrations of ions between the inside and outside the cells

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29
Q

What is the average membrane potential for neurons?

A

-70mV

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30
Q

Is membrane potential higher on the outside or inside of the neuron and why?

A

Higher on the outside since 3 Na+ is transported out whilst 2 K+ is transported in resulting in a higher charge on the outside

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31
Q

What does the NERNST equation calculate?

A

The equilibrium potential for each ion

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32
Q

What causes an electro-chemical gradient across a neuron membrane for each ion?

A

An electrical gradient is formed due to ions being charged and differences in their concentrations across a membrane

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33
Q

What is the Nernst equation?

A

EIon = RT/ZF x ln([ion]in/[ion]out)

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34
Q

In the Nernst equation, what does Z and F represent?

A 
Z = charge
F = Faraday's constant
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35
Q

What are voltage-gated ion channels?

A

Ion channels across a membrane that respond to changes in electrical gradient across a cell membrane

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36
Q

What are the ‘voltage-sensors’ on a voltage-gated ion channel?

A

A series of charged amino acids

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37
Q

When do Na+ channels open (what voltage)?

A

-55mV

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38
Q

When are voltage-gated K+ channels opened?

A

At positive voltages

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39
Q

What are the 3 states that voltage-gated ion channels can exist in?

A

Open, inactivated then closed

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40
Q

Where are ion channels distributed in a neuron?

A

Throughout it, i.e the soma, dendrites and axons, however the distribution of them is different for each ion

41
Q

What happens when glutamate binds to dendrites?

A

Ionotropic receptors are activated which are linked to ion channels. Na+/Ca2+ channel is opened causing these ions to flow into the dendrite and therefore depolarising the membrane and produce an EPSP.

42
Q

What is a EPSP?

A

Excitatory post-synaptic potential

43
Q

What happens when EPSPs are produced?

A

They travel to the soma where they build up and depolarize the soma more. The voltage change spreads to the axon. If the membrane reaches -55mV, the Na+ channels in the initial segment of the axon open and generate an action potential

44
Q

Give an example of a neurotransmitter that generates inhibitory signals that hyperpolarizes membranes

A

GABA

45
Q

How does the binding of GABA result in hyperpolarisation?

A

The Cl- ion channel is opened causing an influx of Cl- into the cell

46
Q

What is the effect of hyperpolarisation of neuron membranes?

A

Neuronal activity will be dampened since it opposes the initiation of action potentials

47
Q

Describe how an action potential is made

A

When EPSPs build up and reach the action potential threshold (-55mV), the voltage-gated Na+ channels open. The influx of Na+ depolarises the membrane potential promoting more Na+ channels to open. When the membrane potential reaches -30mV, the channels shut and the K+ voltage-gated channels open causing an efflux of K+, repolarizing the cell membrane. (action potential repolarisation phase) so that the potential falls below resting potential. The membrane potential is then restored by Na+/K+ ATPase pumps

48
Q

What is the Na+ equilibrium potential and why is this never reached?

A

+60mV. It isn’t reached as the K+ channels open at +30mV and cause the membrane to repolarise

49
Q

What is the relative refractory period?

A

The period when the membrane is hyperpolarised

50
Q

Why are thin axons more likely to have current leak?

A

They have thin cytoplasm so the current can leak easier

51
Q

What is the myelin sheath and why is it important?

A

It is an electrical insulator and helps to prevent leakage of current along axons. This is important as if the current dissipates, the action potential won’t be spread

52
Q

What cells provide the myelin sheath in the PNS and CNS?

A 
PNS = Schwann cells
CNS = oligodendrocytes
53
Q

What are nodes of Ranvier and what happens at them?

A

Gaps in the myelin sheath, voltage-gated ion channels are clustered and so generate action potentials here. Action potentials jump between the nodes

54
Q

What is saltatory conduction?

A

When action potentials jump between nodes of Ranvier

55
Q

Why is it faster for action potentials to travel across a myelinated axon?

A

The myelin sheath creates nodes of Ranvier allowing saltatory conduction to occur. It also insulates the axons allowing action potentials to be generated faster

56
Q

What is the main class of drugs used to affect action potential generation and give an example?

A

Local anaesthetics, lidocaine

57
Q

Are local anaesthetics acids or bases?

A

Weak bases

58
Q

How does lidocaine work as a local anaesthetic?

A

The unionised form penetrates the axonal membrane. Once inside the cell, some is ionised which then binds to voltage-gated Na+ channels. This prevents Na+ ions passing through the channel inhibiting the firing of action potentials

59
Q

What is neurotransmisison?

A

The process where chemical signals (neurotransmitters) are released from axon terminals at synapses between neurons or between neurons and tissues

60
Q

What is the neuromuscular junction?

A

The synaptic connection between a motor nerve and skeletal muscle

61
Q

What is the neurotransmitter released at the neuromuscular junction?

A

Acetylcholine

62
Q

How is acetylcholine synthesised?

A

In nerve terminals, acetyltransferase synthesises acetylcholine from choline and acetyl CoA

63
Q

Describe what happens at the synaptic cleft after acetylcholine has been synthesised

A

Acetylcholine is transported into membrane-bound vesicles via an ATPase proton pump. These vesicles are then transported to the pre-synaptic membrane and anchored (docking) here. An influx of Ca2+ stimulates the release of the contents of the vesicles via exocytosis. Ach then binds to nicotinic receptors on the post-synaptic membrane

64
Q

What allows docking of the vesicles in the pre-synaptic membrane and what does it result in?

A

Proteins on the surface of the vesicles interact with the pre-synaptic membrane to form a SNARE complex which results in the vesicle being primed to release their contents

65
Q

Where does the influx of Ca2+ ions come from that are the stimulus for releasing Ach from the vesicles

A

After an action potential travels down the axon, it reaches the axon terminal where it opens Ca2+ voltage-gated ion channels.

66
Q

How does the vesicles in the pre-synaptic membrane release their contents?

A

One of the SNARE complex proteins binds to Ca2+ resulting in a conformational change so that the vesicle fuses with the membrane and a pore is formed that allows the secretion of the contents

67
Q

What is exocytosis?

A

The secretion of contents of a vesicle by fusion with the membrane

68
Q

What is the end plate?

A

The post-synaptic membrane on the muscle of the neuromuscular junction

69
Q

What happens when 2 molecules of Ach bind to the nicotinic receptors on the post-synaptic cleft?

A

The ion channel opens allowing the influx of Na+ ions and some efflux of K+ ions.

70
Q

What is end plate potential

A

Depolarisation of the end plate as a result of more Na+ coming into the cell and less K+ leaving the cell (the membrane becomes more positive)

71
Q

What is the role of acetylcholinesterase on the post-synaptic membrane?

A

It cleaves acetylcholine into choline and acetate, the choline is transported back into the pre-synaptic terminal to synthesise more Ach and the acetate diffuses into the bloodstream and is excreted

72
Q

What happens in excitation-contraction coupling?

A

Neurotransmission at the neuromuscular junction causes skeletal muscle contraction

73
Q

What causes an action potential at the post-synaptic membrane?

A

When the EPP reaches a threshold, it activates voltage-gated Na+ channels outside of the end plate causing a rapid influx of Na+ and depolarisation of the membrane

74
Q

What do action potentials generated on the post-synaptic membrane travel down to reach skeletal muscle

A

T-tubules

75
Q

What receptors are found along T-tubules that act as voltage sensors?

A

Dihydropyridine receptors

76
Q

What happens when dihydropyridine receptors are activated by action potentials?

A

They promote the release of Ca2+ ions via ryanodine receptors from the sarcoplasmic reticulum into the cytoplasm which stimulates muscle contraction

77
Q

What are the 2 types of filaments that make up muscle?

A

Actin and myosin

78
Q

How is tropomyosin attached to actin filaments in resting state?

A

It is spiralled around it, covering the binding sites for myosin

79
Q

What holds the resting structure of myosin?

A

The troponin complex which contain troponin C

80
Q

What happens to tropomyosin when an action potential is generated and Ca2+ is released?

A

Ca2+ binds to troponin C which changed the conformation of tropomyosin C so that the actin
binding sites are revealed

81
Q

Describe how myosin and actin interact after the binding site has been revealed

A

The head group on myosin binds to ATP which is then hydrolysed to ADP + P so that it can bind to actin by changing the shape of the head group. The P is then released making the head group return to its resting state whilst pulling on the actin filament called the power stroke

82
Q

What are the 2 classes of neuromuscular blockers?

A

Depolarising and non-depolarising

83
Q

What do neuromuscular blockers cause?

A

Skeletal muscle paralysis

84
Q

What is the only depolarising neuromuscular blocker used clinically?

A

Suxamethonium

85
Q

How does suxamethonium work?

A

It is an agonist for the nicotinic receptors on skeletal muscle but causes rapid desensitisation of the receptors leading to paralysis

86
Q

Describe the clinical use of suxamethonium

A

Used to paralyse the larynx (air passage to lungs) to allow tracheal intubation.

87
Q

What is the clinical use of non-depolarising neuromuscular blcokers?

A

Used with general anaesthetics to cause widespread skeletal muscle paralysis during major surgery

88
Q

What type of antagonists are non-depolarising neuromuscular blcokers?

A

competitive, reversible antagonists at nicotinic receptors

89
Q

What are acetylcholinesterase inhibitors?

A

A class of drug that block the enzyme which breaks down acetylcholine

90
Q

Give an example of an acetylcholine inhibitor

A

Neostigmine

91
Q

What type of inhibitor is edrophonium?

A

A competitive, reversible inhibitor of acetylcholinesterase

92
Q

What are organophosphate drugs and what is their use?

A

They bind irreversibly to acetylcholinesterase and have long durations (days) and are largely used as pesticides and also treatment for head lice

93
Q

What is the indication for physostigmine?

A

Treatment of glaucoma (damage to optic nerve). It is applied as eyedrops. It cannot be used orally since it crosses the BBB

94
Q

What is the indication for rivastigmine?

A

Treatment of Alzheimer’s disease where there is a deficit in cholinergic transmission resulting in memory deficiency

95
Q

What is myasthenia gravis?

A

An autoimmune disease where the immune system produces antibodies against acetylcholine receptors at the neuromuscular junction stopping Ach from binding and leads to muscle weakness.

96
Q

What is Lambert Eaton syndrome?

A

An autoimmune system where antibodies are produced against the voltage-gated Ca2+ channels resulting in less Ach being released leading to muscle weakness

97
Q

How can blocking the voltage-gated K+ channels help treat Lambert Eaton syndrome?

A

It reduces the rate at which the pre-synaptic terminal membrane repolarises after an action potential so that the action potential is longer and more acetylcholine is released

98
Q

How does botulinum toxin work (botox)?

A

It interferes with the vesicle fusing with the pre-synaptic membrane resulting in less acetylcholine being released

PHAY0003 (22 decks)

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