Acetylcholine Flashcards

1
Q

What type of NT is ACh?

A

Amine.

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2
Q

How is ACh synthesised?

A

From acetyl CoA and choline, via the enzyme choline acetyltransferase (ChAT).

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3
Q

Which enzyme degrades ACh?

A

Acetylcholinesterase (AChE).

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4
Q

Which transporter is responsible for the reuptake of ACh into the presynaptic terminal?

A

Choline transporter (CHT1).

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5
Q

Where is choline found?

A

In high concentrations in the presynaptic terminal.

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6
Q

What are the two primary roles of ACh?

A

Elicits muscle contractions at the NMJ.
Acts as a neuromodulator for memory and sleep.

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7
Q

Name the three locations of cholinergic nuclei.

A

Nucleus basalis of Meynert.
Medial septum.
Brainstem.

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8
Q

Cell bodies in the nucleus basalis of Meynert and medial septum are vital to what?

A

Normal cognition and memory.

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9
Q

Where does the nucleus basalis of Meynert project to?

A

Cortex.

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10
Q

Where does the medial septum project to?

A

Hippocampus.

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11
Q

Cell bodies in the brainstem are important for what?

A

Sleep and motor control.

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12
Q

Where do cell bodies in the brainstem project to?

A

Diencephalon and basal ganglia.

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13
Q

From where and when are neuromodulators typically released?

A

Released from varicosities during en passant transmission.

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14
Q

Name two ACh agonists.

A

Nicotine.
Muscarine.

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15
Q

Name the five subunits of nicotinic acetylcholine receptors (nAChRs).

A

Alpha.
Beta.
Gamma.
Delta.
Epsilon.

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16
Q

How many alpha nAChR subunits are there?

A

10.

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17
Q

How many beta nAChR subunits are there?

A

4.

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18
Q

Which ions are nAChRs permeable to?

A

Sodium.
Potassium.
Certain subunit combinations confer calcium permeability too.

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19
Q

Describe the structure of nAChRs.

A

5 transmembrane spanning subunits couple together to form the ion channel complex.
Each subunit consists of four membrane-spanning alpha helices.
Can be homomeric or heteromeric.

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20
Q

Describe how functional nAChRs are widely distributed.

A

Distributed across:
Different neuron types.
Different brain regions.
Differentially localised within a neuron, on the soma, dendrites or synaptic terminals.

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21
Q

What does the diverse distribution of nAChRs suggest?

A

Modulation of plasticity and activity at a network level more than linear regulation of individual synaptic pathways.

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22
Q

How do nAChRs modulate NT release?

A

nAChRs are present on the presynaptic terminals of other NT systems.

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23
Q

What is the importance of homomeric alpha-7 nAChR signalling?

A

Can enhance induction of LTP in the hippocampus.
Promotes maturation and survival of adult-born neurons.
Transform GABAergic currents from excitatory in early development to inhibitory later in development.

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24
Q

What do defects in cholinergic signalling cause?

A

Impairments in learning and memory.

25
Q

Which two types of synapses most often contain nAChRs?

A

Glutamatergic or GABAergic.

26
Q

What type of receptor are muscarinic ACh recpetors (mAChRs)?

27
Q

Name the five subtypes of mAChRs.

28
Q

What is atropine?

A

A competitive and reversible antagonist of mAChRs.

29
Q

What is the main role of mAChRs?

A

Mediate the neuroeffector junction of the PNS.

30
Q

Which mAChR subtypes are highly expressed in the brain?

A

M1, M2 and M4.

31
Q

Which G-protein couples to M1, M3 and M5 mAChRs?

32
Q

Which G-protein couples to M2 and M4 mAChRs?

33
Q

Describe the mechanism of action for M1, M3 and M5 mAChRs.

A

Activates phospholipase C, IP3 and DAG.
Increases calcium ion conductance.
Upregulates MAP kinases.

34
Q

Describe the mechanism of action for M2 and M4 mAChRs.

A

Inhibits adenylyl cyclase to reduce levels of cAMP.
Downregulates MAP kinases.
Decreases calcium ion conductance.

35
Q

Describe the two main roles of M1 mAChRs.

A

Gut motility and gastric secretions.
Attenuate potassium conductance to produce excitatory effects at the ganglia.

36
Q

Why does an M2 mAChR produce mainly inhibitory effects?

A

Produces an increase in potassium and a decrease in calcium conductance.

37
Q

What is the role of M2 mAChR in the heart?

A

Reduces heart rate and contraction due to closure of calcium channels.

38
Q

Which three roles are M3 mAChRs involved in?

A

Contribute to smooth muscle contraction in the gastrointestinal and urinary tracts.
Role in bronchoconstriction and vasodilation.
Help to stimulate glandular secretions.

39
Q

Which pathway is an important source of intracellular calcium ions?

A

PIP2-IP3 pathway.

40
Q

What are the two components of the stress response?

A

Autonomic.
Neuroendocrine.

41
Q

Which molecule mediates the autonomic stress response?

A

Adrenaline.

42
Q

Which molecule mediates the neuroendocrine stress response?

43
Q

List three symptoms of the autonomic stress response.

A

Increased heart rate and breathing.
Heightened senses and alertness.
Focused attention.

44
Q

List three symptoms of the neuroendocrine stress response.

A

Increase in blood glucose.
Suppressed immune function.
Stops digestion.

45
Q

What is the role of the ANS?

A

It regulates the viscera of the body, e.g. secretions of certain glands, heart rate, and peristalsis.

46
Q

Define peristalsis.

A

Contraction of smooth muscle in the digestive tract.

47
Q

Which subsection of the ANS is involved in the autonomic stress response?

48
Q

Which subsection of the ANS is involved in the neuroendocrine stress response?

49
Q

Describe the mechanism of action of nicotine in the SNS.

A

Stimulates NA release by activating mAChRs localised on peripheral postganglionic neurons.
Increases heart rate and blood pressure.

50
Q

Define the neuromuscular junction (NMJ).

A

A specialised site that connects the terminal of a motor neuron axon to skeletal muscle.

51
Q

How are muscle fibres innervated?

A

Each muscle fibre is innervated and controlled by a single motor neuron.

52
Q

Where is the motor neuron cell body located?

A

Within the spinal cord.

53
Q

What is the motor end plate?

A

The site where a motor neuron axon synapses with a muscle fibre.

54
Q

Where does ACh bind to once it has been released from the presynaptic motor neuron?

A

Postsynaptic nAChRs concentrated in the folded membrane at the motor end plate.

55
Q

Via which process is ACh released from the presynaptic motor neuron terminal?

A

Calcium-dependent exocytosis.

56
Q

What is the role of the junctional folds in the motor end plate?

A

Allows ACh to accumulate to depolarise the membrane (sarcolemma) of the muscle fibre.

57
Q

How do neurotoxins inhibit ACh release?

A

They interfere with the SNARE proteins that mediate vesicle fusion.
This prevents fusion of synaptic vesicles with the presynaptic membrane, thereby inhibiting exocytosis.

58
Q

What is the cause of myasthenia gravis?

A

Autoantibodies block nAChRs at the NMJ, leading to reduced muscle contraction.

59
Q

Define myasthenia gravis.

A

It is an autoimmune disorder characterised by weakness of skeletal muscles.