Nerves and Neurotransmitters Flashcards

(98 cards)

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
What in neuron membranes allows the ionic concentrations to be maintained?
Pumps and ion channels
26
Describe what the Na+/K+ ATPase pump does
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
27
When are leak K+ channels open on neurons?
At rest
28
Why is a membrane potential generated on neurons?
There is a difference in concentrations of ions between the inside and outside the cells
29
What is the average membrane potential for neurons?
-70mV
30
Is membrane potential higher on the outside or inside of the neuron and why?
Higher on the outside since 3 Na+ is transported out whilst 2 K+ is transported in resulting in a higher charge on the outside
31
What does the NERNST equation calculate?
The equilibrium potential for each ion
32
What causes an electro-chemical gradient across a neuron membrane for each ion?
An electrical gradient is formed due to ions being charged and differences in their concentrations across a membrane
33
What is the Nernst equation?
EIon = RT/ZF x ln([ion]in/[ion]out)
34
In the Nernst equation, what does Z and F represent?
``` Z = charge F = Faraday's constant ```
35
What are voltage-gated ion channels?
Ion channels across a membrane that respond to changes in electrical gradient across a cell membrane
36
What are the 'voltage-sensors' on a voltage-gated ion channel?
A series of charged amino acids
37
When do Na+ channels open (what voltage)?
-55mV
38
When are voltage-gated K+ channels opened?
At positive voltages
39
What are the 3 states that voltage-gated ion channels can exist in?
Open, inactivated then closed
40
Where are ion channels distributed in a neuron?
Throughout it, i.e the soma, dendrites and axons, however the distribution of them is different for each ion
41
What happens when glutamate binds to dendrites?
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
What is a EPSP?
Excitatory post-synaptic potential
43
What happens when EPSPs are produced?
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
Give an example of a neurotransmitter that generates inhibitory signals that hyperpolarizes membranes
GABA
45
How does the binding of GABA result in hyperpolarisation?
The Cl- ion channel is opened causing an influx of Cl- into the cell
46
What is the effect of hyperpolarisation of neuron membranes?
Neuronal activity will be dampened since it opposes the initiation of action potentials
47
Describe how an action potential is made
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
What is the Na+ equilibrium potential and why is this never reached?
+60mV. It isn't reached as the K+ channels open at +30mV and cause the membrane to repolarise
49
What is the relative refractory period?
The period when the membrane is hyperpolarised
50
Why are thin axons more likely to have current leak?
They have thin cytoplasm so the current can leak easier
51
What is the myelin sheath and why is it important?
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
What cells provide the myelin sheath in the PNS and CNS?
``` PNS = Schwann cells CNS = oligodendrocytes ```
53
What are nodes of Ranvier and what happens at them?
Gaps in the myelin sheath, voltage-gated ion channels are clustered and so generate action potentials here. Action potentials jump between the nodes
54
What is saltatory conduction?
When action potentials jump between nodes of Ranvier
55
Why is it faster for action potentials to travel across a myelinated axon?
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
What is the main class of drugs used to affect action potential generation and give an example?
Local anaesthetics, lidocaine
57
Are local anaesthetics acids or bases?
Weak bases
58
How does lidocaine work as a local anaesthetic?
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
What is neurotransmisison?
The process where chemical signals (neurotransmitters) are released from axon terminals at synapses between neurons or between neurons and tissues
60
What is the neuromuscular junction?
The synaptic connection between a motor nerve and skeletal muscle
61
What is the neurotransmitter released at the neuromuscular junction?
Acetylcholine
62
How is acetylcholine synthesised?
In nerve terminals, acetyltransferase synthesises acetylcholine from choline and acetyl CoA
63
Describe what happens at the synaptic cleft after acetylcholine has been synthesised
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
What allows docking of the vesicles in the pre-synaptic membrane and what does it result in?
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
Where does the influx of Ca2+ ions come from that are the stimulus for releasing Ach from the vesicles
After an action potential travels down the axon, it reaches the axon terminal where it opens Ca2+ voltage-gated ion channels.
66
How does the vesicles in the pre-synaptic membrane release their contents?
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
What is exocytosis?
The secretion of contents of a vesicle by fusion with the membrane
68
What is the end plate?
The post-synaptic membrane on the muscle of the neuromuscular junction
69
What happens when 2 molecules of Ach bind to the nicotinic receptors on the post-synaptic cleft?
The ion channel opens allowing the influx of Na+ ions and some efflux of K+ ions.
70
What is end plate potential
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
What is the role of acetylcholinesterase on the post-synaptic membrane?
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
What happens in excitation-contraction coupling?
Neurotransmission at the neuromuscular junction causes skeletal muscle contraction
73
What causes an action potential at the post-synaptic membrane?
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
What do action potentials generated on the post-synaptic membrane travel down to reach skeletal muscle
T-tubules
75
What receptors are found along T-tubules that act as voltage sensors?
Dihydropyridine receptors
76
What happens when dihydropyridine receptors are activated by action potentials?
They promote the release of Ca2+ ions via ryanodine receptors from the sarcoplasmic reticulum into the cytoplasm which stimulates muscle contraction
77
What are the 2 types of filaments that make up muscle?
Actin and myosin
78
How is tropomyosin attached to actin filaments in resting state?
It is spiralled around it, covering the binding sites for myosin
79
What holds the resting structure of myosin?
The troponin complex which contain troponin C
80
What happens to tropomyosin when an action potential is generated and Ca2+ is released?
Ca2+ binds to troponin C which changed the conformation of tropomyosin C so that the actin binding sites are revealed
81
Describe how myosin and actin interact after the binding site has been revealed
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
What are the 2 classes of neuromuscular blockers?
Depolarising and non-depolarising
83
What do neuromuscular blockers cause?
Skeletal muscle paralysis
84
What is the only depolarising neuromuscular blocker used clinically?
Suxamethonium
85
How does suxamethonium work?
It is an agonist for the nicotinic receptors on skeletal muscle but causes rapid desensitisation of the receptors leading to paralysis
86
Describe the clinical use of suxamethonium
Used to paralyse the larynx (air passage to lungs) to allow tracheal intubation.
87
What is the clinical use of non-depolarising neuromuscular blcokers?
Used with general anaesthetics to cause widespread skeletal muscle paralysis during major surgery
88
What type of antagonists are non-depolarising neuromuscular blcokers?
competitive, reversible antagonists at nicotinic receptors
89
What are acetylcholinesterase inhibitors?
A class of drug that block the enzyme which breaks down acetylcholine
90
Give an example of an acetylcholine inhibitor
Neostigmine
91
What type of inhibitor is edrophonium?
A competitive, reversible inhibitor of acetylcholinesterase
92
What are organophosphate drugs and what is their use?
They bind irreversibly to acetylcholinesterase and have long durations (days) and are largely used as pesticides and also treatment for head lice
93
What is the indication for physostigmine?
Treatment of glaucoma (damage to optic nerve). It is applied as eyedrops. It cannot be used orally since it crosses the BBB
94
What is the indication for rivastigmine?
Treatment of Alzheimer's disease where there is a deficit in cholinergic transmission resulting in memory deficiency
95
What is myasthenia gravis?
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
What is Lambert Eaton syndrome?
An autoimmune system where antibodies are produced against the voltage-gated Ca2+ channels resulting in less Ach being released leading to muscle weakness
97
How can blocking the voltage-gated K+ channels help treat Lambert Eaton syndrome?
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
How does botulinum toxin work (botox)?
It interferes with the vesicle fusing with the pre-synaptic membrane resulting in less acetylcholine being released