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PHAR232 > Module 4: ANS Pharmacology > Flashcards

Module 4: ANS Pharmacology Flashcards

1
Q

What is acetylcholine?

A

The neurotransmitter in the parasympathetic nervous system, and in the brain (learning, memory, cognition)

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2
Q

How is ACh transported?

A

VAchT (vesicular ACh Transporter) using H+-ATPase pump

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3
Q

What is the rate limiting step in ACh signalling?

A

Availability of choline

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4
Q

What is the source of choline in the brain?

A

Mostly recycled ACh or catabolism phosphatidyl-choline.

Small amount grosses BBB but does not readily cross

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5
Q

What causes the mobilisation of ACh vesicles towards the synaptic terminal?

A

An influx of calcium, triggered by an influx of sodium as the membrane potential travels down the Neuron

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6
Q

What is AChE?

A

Acetylcholinesterase - enzyme that destroys ACh in the synaptic space to control how long the ACh can exert its effect

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7
Q

What are autoreceptors?

A

“Eyes of the synapse”

Allows the pre-synaptic terminal to monitor how much ACh released.

mAChRs - muscarinic ACh receptors.

They inhibit further ACh release as feedback regulation

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8
Q

What are nAChRs?

A

Nicotinic ACh receptors - presynaptic - promote further ACh release and compete with mAChRs.

Not present on all synapses.

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9
Q

How do botulinum toxins work?

A

They are enzymes that destroy proteins responsible for vesicles release. Therefore inhibit ACh release.

It can stop muscle spasms in cerebral palsy etc

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10
Q

What are the core steps at any synapse?

A
  1. Dedicated neurotransmitter synthesis
  2. A rate-limiting step for control of synaptic action (ie choline availability)
  3. A method of rapid termination of signal (ie AChE)
  4. Means of feedback regulation (ie auto regulation)
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11
Q

What is a cholinergic Neuron?

A

A Neuron that released ACh

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12
Q

How many types of mAChRs are there?

A

Five.

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13
Q

What are the 5 subtypes of mAChRs?

A

M1, M3, M5 all activate phospholipase C.

M1- neutrons
M3 - glands/smooth muscle
M5- CNS/ salivary glands

M2 and M4 use G proteins to inhibit AdCy for cell inhibition.
M2 - cardiac
M4 - CNS

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14
Q

What type of receptors are mAChRs?

A

Metabotropic

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15
Q

what are some effects of muscarinic receptors?

A
  • cardiovascular effects (slows HR, decrease CO, vasodilation
  • smooth muscle (increase peristalsis, bronchoconstriction)
  • secretions (promotes sweating, salivation, exocrine glands)
  • eye (constricts pupillae & ciliary muscles)
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16
Q

What type of receptor is nAChRs?

A

Ionotropic

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17
Q

What is the general structure of nAChRs?

A

5 subunits in pore formation. Alpha, beta and gamma subunits - BUT some have been found with all alpha subunits

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18
Q

What action does nAChR cause?

A

Sodium influx drives the cell to threshold - to activate voltage gated channels. Results in cell excitation

19
Q

What are the effects of nicotinic receptors?

A
  • skeletal muscles (increases contraction at neuromuscular junction)
  • autonomic ganglia (complex effects both sympathetic and parasympathetic - impact depends which system is in charge of that organ. Also adrenal gland)
  • CNS (motor cortex, basal ganglia, excitatory neurotransmission)
20
Q

What is parasympathomimetic?

A

Drugs that mimic or enhance the parasympathetic nervous system. They target muscarinic receptors but not nicotinic (muscarinic agonist)

21
Q

What does the parasympathetic nervous system use to target organs?

A

Muscarinic receptors

22
Q

What are uses and side effects of parasympathomimetics?

A

Use for glaucoma treatment.

Side effects are parasympathetic activation - drooling, sweating, urination, defecation etc

23
Q

What are acetylcholinesterase inhibitors?

A

They block acetylcholinesterase therefore action of ACh is prolonged.

Could be classified as parasympathomimetic, but aren’t because they purely target ACherase

24
Q

How do muscarinic antagonists work?

A

Blocks parasympathetic nervous system activity. Also referred to as parasympatholytic.

Results in inhibition of glandular secretions (reduced saliva) and alter heart rate. Dilates pupil and impair near vision, inhibit Gi motility, road smooth muscle ie bronchioles and bladder

25
Q

What is a catecholamine?

A

A group of compounds including noradrenaline, adrenaline, dopamine

26
Q

What is another name for adrenaline?

A

Epinephrine

27
Q

What is the rate limiting step in catecholamine biosynthesis?

A

Tyrosine hydroxylase.

However, there is normally a saturated amount of tyrosine, but cofactors are the rate limiting factor.

28
Q

What type of receptor are adrenergic receptors?

A

Metabotropic

29
Q

what is the basic structure of adrenergic receptors?

A

7 transmembrane domains with extra cellular N terminus, 3rd intercellular loop and intracellular C terminus (but different to normal GPCRs)

30
Q

What are the different types of adrenergic receptors?

A

Alpha and beta.

31
Q

What is the difference between noradrenaline and adrenaline?

A

Noradrenaline is a neurotransmitter

Adrenaline is a hormone .

Interact differently with different receptors (ie NA has very small effect on B2 receptors vs adrenaline

32
Q

Where are the B1 and B2 adrenergic receptors found?

A

B1 in the heart, B2 in the lungs

33
Q

What is the means of rapid termination of signal in noradrenergic synapses?

A

It is transported out of the synapse by NET (norepinephrine transporter) back into the pre-synaptic Neuron (major) and EMT into postsynaptic Neuron (minor)

34
Q

How are catecholamines synthesised?

A 
Tyrosine
(Tyrosine hydroxylase)
DOPA
Dopamine
Noradrenaline
Adrenaline
35
Q

What is a neuromodulator?

A

A compound that fine tunes signals (can be positive or negative)

36
Q

What is the significance of noradrenaline vesicles having 4 molecules of ATP per molecule of NA?

A

It acts as a built-in neuromodulator

37
Q

What effects do catecholamines have?

A

(Mediated by adrenergic receptors)

  • dilate pupils
  • constrict blood vessels (a1)
  • dilate blood vessels (a2 & B2)
  • inhibit histamine release from mast cells
  • decrease gut motility
  • goosebumps
38
Q

What is the effect of dopamine in the periphery and central systems?

A

Periphery - partial agonist of B1, works in kidneys

Central - motor activity, modulate behaviour, mediate reward pathway, control of pituitary gland secretions

39
Q

What are 2 categories of adrenergic drugs?

A

Sympathimimetic (mimic sympathetic)

Sympatholytic (oppose/block sympathetic)

40
Q

How is adrenaline released?

A

It is released from adrenal medulla (by ACh acting on nAChRs in sympathetic chain)

41
Q

What is the effect of adrenaline?

A

Increase HR & contraction force (B1)

Vasoconstriction of majority of blood vessels (A1)

Vasodilation if some key blood vessels (B2)

Promote renin release from kidneys (B1)

42
Q

What are the side effects of adrenaline?

A

Primary is cardiovascular - tachycardia, elevated BP vasoconstriction leading to ischaemia.

43
Q

What are mixed-action sumpathomimetics?

A

Drugs that activate adrenergic receptors & promote NA release

44
Q

What are indirect-acting sympathomimetics?

A

Drugs that compete with NA at uptake proteins and vesicles transporters - prolong Na effect at synapse

PHAR232 (5 decks)

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