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Pharmacology > S1: Effect of Drugs on Synaptic Transmission > Flashcards

S1: Effect of Drugs on Synaptic Transmission Flashcards

1
Q

What are the criteria of a neurotransmitter?

A
  1. It must be synthesised in nerves- genes present in the nucleus of the cell body
  2. Released from nerves: present in vesicles which enables easy and concentrated release from nerve
  3. Identity of action: stimulating nerve has same effect as applying NT
  4. Receptors for NT: use of agonist and antagonist
  5. Mechanisms present to terminate action of NT- uptake transporters and enzymes
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2
Q

Name the 3 types neurotransmitter in the CNS

A

Amino acids
Amines
Neuromodulators/ Neurotrophic agents

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3
Q

Describe chemical transmission (site of drug action)

A
  1. Synthesis of NT
  2. Storage of NT in vesicles
  3. Arrival of AP at synaptic terminal
  4. Depolarisation of terminal to activate VGCC and influx of Ca2+ ions into presynaptic neurone
  5. Ca2+ dependent release of NT
  6. NT binds to receptor inducing response
  7. Termination (uptake/breakdown of NT)
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4
Q

How can drugs block the propagation of AP?

A

They stop it by blocking voltage dependent Na+ channels, which prevent AP generation and propagation along the axon. Therefore it will stop the presynaptic terminal from being depolarisation and no Ca2+ influx can occur. Synaptic transmission is therefore inhibited.

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5
Q

Examples of drugs that stop AP transmission

A

Local anaesthetics e.g. lignocaine
Prevents AP conduction and synaptic transmission in sensory nerves so stops input to brain that code for pain. Hence the individual has no sensation for pain.

Anti-epileptic e.g. phenytoin
This prevents excessive synaptic transmission during the high frequency firing in the CNS associated with seizures

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6
Q

How can drugs prevent influx of Ca2+?

A

These drugs are very potent blockers of synaptic transmission.

The rational behind them is that they block voltage dependent Ca2+ channels and it will prevent Ca2+ influx into the synaptic bouton. The neurotransmitter will therefore will not be released and this inhibits synaptic transmission.

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7
Q

Examples of drugs that inhibit VGCC

A

Analgesics e.g. zincinotide

GABApentin

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8
Q

What happens if substrate levels are increased and NT is prevented from being broken down?

A

Concentration of NT increases

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9
Q

How is dopamine made?

A

L-tyrosine is converted into DOPA by tyrosine hydroxylase

DOPA is converted to dopamine by DOPA decarboxylase (DDC)

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10
Q

What converts L-tyrosine to DOPA

A

Tyrosine hydroxylase

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11
Q

What enzyme converts DOPA to Dopamine?

A

DOPA decarboxylase (DDC)

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12
Q

What 2 things break down Dopamine?

A

Monoamine oxidase (MAO)

Catechil-O-methyl transferase (COMT)

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13
Q

What happens if dopa levels are increased and MAI/COMT inhibitors are added?

A

Dopamine levels are increased

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14
Q

What does levodopa (substrate) do?

A

It is prescribed with a peripheral DDC inhibitor (does not cross blood brain barrier) and Carbidopa (prevents breakdown of levodopa)

This prevents synthesis of dopamine in systemic system as DOPA cannot be converted to dopamine.

This allows DOPA from our body to travel to our brain and be converted by DDC therefore….

Maximising dopamine synthesis in the brain

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15
Q

Explain the mechanism of Clostridum Botulinum?

A

Bacteria produces toxin called botulism.

Toxin enters terminals and defeated vesicles containing acetylcholine.

ANS and somatic motor fibres are inhibited

This causes symptoms of muscle paralysis and death

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16
Q

List some uses of Botox

A

Very low concentrations of Botox are used to produce local paralysis of muscles
For example, cosmetic uses to reduce wrinkles

Clinical uses involve preventing excess sweat by decreasing Ach acting on sweat glands (exception in sympathetic response)

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17
Q

Mechanism of Amphetamine

A

It’s binds to and reverses the action of Monoamine uptake transporters

This causes release of noradrenaline, dopamine and serotonin

It increases the action of the sympathetic nervous system e.g. pupils to dilate

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18
Q

What is ephedrine and what is it used for?

A

It is a derivative of amphetamine

It is widely used as a decongestant as it causes vasoconstriction of nasal blood vessels

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19
Q

Explain the mechanism of Guanethidine?

A

Competes with noradrenaline for inclusion into vesicles and prevents release of noradrenaline

20
Q

Explain the mechanism of clonidine/a methyl-DOPA?

A

Stimulate the presynaptic a2 receptors and reduces noradrenaline release

21
Q

What is clonidine/a-methyl-DOPA used for (clinical)?

A

Hypertensive emergencies

22
Q

How do anti-cholinesterases (AchE) work?

A

Acetylcholinesterases breaks down acetylcholine.
Anti-cholinesterases are drugs that enhance cholinergic transmission do more Ach remains.
This will cause increased parasympathetic actions e.g. bradycardia, bronchoconstriction

It will also cause an increase in activity at NMJ causing muscle twitching and possibly paralysis

23
Q

Beta-bungarotoxin prevents Ach release.

What animal releases this toxin?

A

Snake venom

24
Q

How are some drugs (e.g. AchE) classified ?

A

They are classified based in their duration/mode of action

  • short acting
  • medium acting
  • long acting: irreversible
25
Q

Where is acetylcholine synthesised?

A

NMJ
Preganglionic fibres
Parasympathetic post ganglionic fibres
CNS

26
Q

How is acetyl choline synthesised?

A

Choline + acetyl coA ———-> Acetyl choline + CoA

The enzyme used is choline acetyltransferase

27
Q

What does ChAT stand for?

A

Choline acetyltransferase

28
Q

Where do we get choline?

A

In our diet such as liver and fish

Choline is also taken up by the choline carrier at the presynaptic terminal

29
Q

What produces acetyl coA?

A

Cellular respiration

30
Q

How is the cholinergic synapse terminated?

A

Released acetylcholine is broken down by acetylcholinesterase (AchE) located at the post synaptic membrane

Ach—————-> choline + acetate
AchE

31
Q

Name the locations where adrenaline and noradrenaline are synthesised?

A

Sympathetic post ganglionic fibres
CNS
Adrenal medulla

32
Q

How are noradrenaline and adrenaline synthesised?

A

From dopamine!

Dopamine is converted to noradrenaline from dopamine hydroxylase

Noradrenaline is converted to adrenaline by PNMT (adrenal medulla)

33
Q

What is the rate limiting step in the production of NA/A?

A

The first step with tyrosine hydroxylase

34
Q

How is noradrenaline stored?

A

NA is stored in vesicles in a complex of ATP.

This is because ATP is also a neurotransmitter at noradrenergic synapses

35
Q

Explain the mechanism of reserpine

A

It’s a drug that distrupts the complex between NA/ATP so NA leaks out into the cytoplasm.
This reduces the ability of vesicles to take up NA. This progressively depleted the NA available for release so reduces adrenergic transmission.

36
Q

What is the clinical use of reserpine?

A

Early treatment for hypertension

37
Q

What do adrenergic neurone blockers do?

A

Drugs can be used to inhibit release of noradrenaline

38
Q

How is NA removal different to Ach?

A

NA removal is not just enzymatic in the synaptic cleft like Ach
NA is also removed by re-uptake unchanged back into the pre-synaptic terminal

39
Q

Name 2 NA uptake carriers

A

High affinity carrier: Uptake 1 (neuronal sites, ANS,CNS)

Low affinity carrier: Uptake 2 (non-neuronal sites)

40
Q

How is NA removed?

A
  1. NA is recycles back into vesicles
  2. Metabolised by Monamine oxidase (MAO) in neurones
  3. Metabolised by catechol-O-methyltransferase (COMT) in non neuronal sites such as the adrenal medulla
41
Q

How does cocaine/tricyclic anti depressants affect adrenergic transmission?

A

They inhibit Uptake 1 so increase adrenergic transmission

43
Q

How does selective serotonin reuptake inhibitors (SSRIs) work?

A

It increases serotonin in the brain

It is given to patients with depression who have reduces 5-HT (serotonin) levels in the brain
It increases 5-HT as more remains in the cleft increasing neurotransmission of 5-HT

44
Q

Give an example of SSRI

A

Fluoxetine

44
Q

What’s another name for serotonin?

A

5-HT

45
Q

Give examples of monoamine neurotransmitters

A

Serotonin
Dopamine
Noradrenaline

46
Q

What does ziconotide do?

A

It blocks VGCa2+ channels preventing calcium influx into the synaptic bouton and hence neurotransmitter is not released

Pharmacology (13 decks)

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