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Pharmacology > Synaptic Transmission > Flashcards

Synaptic Transmission Flashcards

1
Q

What are the monoamine NTs?

A

Histamine
Serotonin
Melatonin

Dopamine
Norepinephrine
Epinephrine

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2
Q

What are the 5 steps in neurotransmission?

A
  1. NT synthesis
  2. Vesicular storage
  3. Synaptic release
  4. NT receptror binding
  5. Termination of NT action
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3
Q

How can drugs target NT synthesis?

A
  • Therapeutic drugs can inhibit enzymes involved in neurotransmitter production.
  • Precursor loading can be used to generate more NTs and increase NT activity
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4
Q

How do neuropeptides differ from monoamine NTs?

A

They require mRNAs from the nuclear DNA to synthesize and are packed into dense core vesicles in the ER

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5
Q

What is the difference in the trigger for release of NTs and neuropeptides?

A

Neuropeptides need a longer duration of increased Ca2+ to be released as they travel much farther than NTs do.

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6
Q

Can neuropeptides cross the BBB?

A

No

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7
Q

What is the rate limiting enzyme of dopamine synthesis?

A

Tyrosine Hydroxylase

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8
Q

What does the selectivity of a NT drug depend on?

A

Depends on access to target cell type

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9
Q

What is the function of vesicular storage?

A

Storage of neurotransmitters in synaptic vesicles protects them from degradation by cytosolic enzymes.

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10
Q

How does botulinum toxin function?

A

Botulinum toxin degrades SNAREs of the cholinergic neuromuscular junction resulting in skeletal muscle paralysis due to loss of acetylcholine release.

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11
Q

What is the renin angiotensin system?

A

Renin is released from the kidney which converts angiotensinogen from the liver into angiotensin I and ACE from the lung converts angiotensin I into angiotensin II which has effects that will increase BP.

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12
Q

How does amphetamine act on the synapse?

A

It is an indirectly acting drug (do not interact directly with a receptor) that stimulates the release of neurotransmitters in a calcium-independent manner.

It is taken up by re-uptake transporters at the axon terminal and it can activate signaling mechanisms that actually reverse the direction of neurotransmitter transport, resulting in the release of endogenous neurotransmitter back out to the extracellular side of the membrane without any membrane voltage change and calcium influx.

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13
Q

What kinds of drugs allow for the most selective control?

A

Drugs that bind directly to receptors

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14
Q

What are the mechanisms that result in the termination of NT action?

A
  1. Reuptake of the NT
  2. Diffusion of the NT out of the synapse
  3. NT degradation
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15
Q

What is the precursor to E and NE?

A

Dopamine

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16
Q

What is the action of metyrosine?

A

Metyrosine binds to tyrosine hydroxylase, but cannot be transformed to DOPA, and thus decreases production of dopamine.

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17
Q

Metyrosine indication

A

Metyrosine is used in the treatment of hypertension by reducing norepinephrine production.

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18
Q

What is the action of L-DOPA?

A

L-DOPA is a precursor of dopamine and it is used to load up on precursor to increase DOPA production.

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19
Q

What are some negative effects of L-DOPA?

A

DOPA loading can have adverse effects on the cardiovascular system due to enhanced norepinephrine neurotransmission in the peripheral autonomic nerves.

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20
Q

L-DOPA indication

A

It is used to treat Parkinson’s disease in which dopaminergic neurons in the brain are damaged.

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21
Q

What is the action of carbidopa?

A

Carbidopa blocks the conversion of L-DOPA to dopamine.

22
Q

Does carbidopa cross the BBB and what is the effect of this?

A

Carbidopa does not cross the blood brain barrier. It can be used to reduce the cardiovascular side effects of L-DOPA in peripheral adrenergic nerves, and preserve the beneficial effects of L-DOPA treatment for Parkinson’s disease within the CNS.

23
Q

What is the action of reserpine?

A

The vesicular monoamine transporter (VMAT) is blocked by reserpine which results in the depletion of
monoamines (NE, DA, and serotonin).

24
Q

Does reserpine cross the BBB and what is the effect of this?

A

Reserpine can cross the blood brain barrier and block monoamine vesicular uptake in CNS neurons which can contribute to depression.

25
Q

Reserpine indication

A

Hypertension

26
Q

Carbidopa indication

A

Parkinson’s Disease

27
Q

What is the action of beryllium?

A

Bretylium inhibits excitability of the nerve terminal membrane and Ca2+- dependent fusion of the synaptic vesicle with the plasma membrane thus reducing neurotransmitter release. Thus bretylium has specific effects on adrenergic neurotransmission.

28
Q

Bretylium indication

A

This drug is used to reduce ventricular arrhythmia in a hospital setting.

29
Q

What is the function of a and b adrenergic receptors?

A

Activation of pre-synaptic adrenergic receptors on nerve terminals influences neurotransmitter release, a−adrenergic receptors can inhibit, while b−adrenergic receptors can facilitate neurotransmitter release.

30
Q

What is the function of catecholamine-O-methyltransferase (COMT)?

A

Termination of exogenously administered norepinephrine is mediated, in large part, by metabolism in plasma by catecholamine-O-methyltransferase (COMT).

31
Q

What is the function of monoamine oxidase (MAO)?

A

Monoamine oxidase (MAO), is present within the cell cytoplasm and rapidly oxidizes any norepinephrine and dopamine within the cytoplasm that is not transported into synaptic vesicles within time.

32
Q

What is the action of cocaine?

A

Cocaine inhibits re-uptake of monoamines including norepinephrine, dopamine and serotonin.

33
Q

Cocaine indication

A

Analgesia

34
Q

What is the action of tricyclic antidepressants?

A

Tri-cyclic antidepressants block re-uptake of several monoamines.

35
Q

What is the action of selective serotonin re-uptake inhibitors (SSRIs)?

A

Inhibition of serotonin reuptake

36
Q

SSRI indication

A

Depression

37
Q

What are common side effects of the antidepressants?

A

They have significant systemic side effects, particularly in the cardiovascular system, which is richly innervated by noradrenergic neurons.

38
Q

Why are exogenous catecholamines not very effective?

A

COMT degradation

39
Q

What is the action of phenylephrine?

A

Direct agonist of adrenergic receptors

40
Q

Phenylephrine indication

A

Hypotension in surgery

41
Q

What is the action of MAO inhibitors?

A

Increase catecholamines in the cytoplasm by blocking MAO’s activity to degrade them.

42
Q

MAO inhibitor indication

A

Depression

43
Q

How is MAO inhibition used to treat depression?

A

As norepinephrine accumulates in the cytoplasm, the transporter protein reverses direction leading to expulsion of norepinephrine into the synapse.

44
Q

What is a problem with tyramine and MAO inhibitors?

A

When MAOs are inhibited, such as during treatment for depression, ingested tyramine accumulates and is transported into adrenergic cells where it competes with
norepinephrine for transport into synaptic vesicles resulting in even higher levels of cytoplasmic norepinephrine than with MAO inhibitors alone.

The cytoplasmic accumulation of norepinephrine can reverse the concentration gradient across the plasma membrane and cause the reversal of the reuptake transporter. The resulting excessive release of norepinephrine can lead to a hypertensive crisis due to excessive vasoconstriction by norepinephrine in the periphery.

45
Q

Why are neuropeptides not good for use in the CNS?

A

They cannot cross the blood brain barrier.

46
Q

What are examples of non-peptide opioid receptor antagonists?

A

Naloxone

Naltrexone

47
Q

What is the action of naloxone?

A

Blocks opioid receptors in the CNS

48
Q

Naloxone indication

A

Reversing opioid overdose

49
Q

What is the difference between naltrexone and naloxone?

A

Naltrexone has a longer duration of action and is used in the treatment of opiate addiction and alcoholism.

50
Q

What is the action of ACE inhibitors (-prils)?

A

Inhibit ACE and prevent conversion of angiotensin I to II

51
Q

ACE inhibitor indication

A

Hypertension

Pharmacology (74 decks)

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