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Brain and Behavior Part 2 > Neuropharm of Catecholamines > Flashcards

Neuropharm of Catecholamines Flashcards

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1
Q

Sympathetics use catecholamines with one exception. What’s the exception?

A

Sweat gland innervation uses Ach (not important for this class, but relevant for boards)

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2
Q

What 4 primary neurotransmittters are used in the sympathetic nervous system (SNS)?

A

Epinephrine, NE, dopamine, 5-HT

we don’t know if dopamine and 5-HT are really involved in the SNS, though

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3
Q

What are 3 contransmitters in the SNS?

A

ATP, Galanin, and Neuropeptide Y

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4
Q

Review: What are the 4 defining properties of a neurotransmitter?

A

Specific synthesis mechanism.
Mechanism to store and release.
Recognition site.
Inactivation process.

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5
Q

From what amino acid are epinephrine and norepinephrine synthesized?

A

Tyrosine.

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6
Q

What are the intermediates between tyrosine and epinephrine?

A

Tyrosine -> Dopa -> Dopamine -> Norepinephrine -> Epinephrine

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7
Q

What enzyme converts tyrosine to dopa?

A

Tyrosine hydroxylase (don’t confuse with tryptophan hydroxylase)

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8
Q

What enzyme converts Dopa to dopamine?

A

L-aromatic amino acid decarboxylase (LAAD)

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9
Q

What enzyme converts dopamine to norepinephrine?

A

Dopamine beta-hydroxylase

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10
Q

What enzyme converts norepinephrine to epinephrine?

A

Phenylethanolamine N-methyltransfersase (PNMT)

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11
Q

What’s the rate-limiting step for getting from tyrosine to NE? Enzyme used?

A

Conversion of Tyr to Dopa by Tyrosine hydroxylase.

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12
Q

What enzymes does the substantia nigra lack?

A

The substantia nigra wants this pathway to stop at dopamine, so it won’t have Dopamine beta-hydoxylase and PNMT.

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13
Q

How does stress affect Tyrosine hydroxylase?

A

Stress leads to upregulation of the gene that encodes the enzyme.

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14
Q

What do biosynthetic vesicles for catecholamines contain? (5 things)

A

Catecholamines, ATP, Dopamine beta-hydroxylase, ascorbic acid, and NPY.

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15
Q

What sort of negative feedback fro catecholamine synthesis is there?

A

Dopamine inhibits Tyrosine hydroxylase.

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16
Q

How does the adrenal medulla produce both epinephrine and NE?

A

2 different cell types. One of them doesn’t have PNMT, one does.

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17
Q

How does stress affect PMNT?

A

Stress, specifically cortisol, leads to increased transcription of the gene for PNMT.

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18
Q

How do catecholamines get into vesicles for storage/secretion?

A

VMAT (vesicle monoamine transporter) - recall that this is also used for 5-HT.

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19
Q

Review?: What does Ca++ specifically interact with on vesicles to trigger fusion and release?

A

VAMPs (vesicle-associated membrane proteins)

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20
Q

What are the 2 different autoreceptors for catecholamines on the presynaptic nerve terminal? What effect does each have?

A

alpha 2 adrenergic: inhibitory for NE release
beta adrenergic: stimulatory for NE release
(i.e. both negative and positive feedback)

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21
Q

Review: What second messengers do Gs, Gi, and Gq use?

A

Gs: increase cAMP
Gi: decrease cAMP
Gq: increase cytosolic Ca++

22
Q

Review: What class of receptors are adrenoreceptors?

A

GPCRs

23
Q

What type of G protein do alpha-1 receptors have? What catecholamine(s) do they bind?

A

Gq

Bind both NE and Epi

24
Q

What type of G protein do alpha-2 adrenoeceptors have? What catecholamine(s) do they bind?

A

Gi

Bind both NE and Epi

25
Q

What type of G protein do both beta-1 and beta-2 adrenoreceptors have? What catecholamine(s) do they bind?

A

Both use Gs.
Beta-1 binds both NE and Epi
Beta-2 only binds Epi

26
Q

Which adrenoreceptor only binds epinephrine (and not NE)?

A

Beta-2

27
Q

What are the 2 major systems for neurotransmitter reuptake? Briefly describe them. (Where? How fast? Capacity?)

A

Uptake 1: Uptake into nerve terminals. Fast (high affintiy), low capacity.
Uptake 2: Extra-neuronal uptake. Slow (low-affinity), high capacity.

28
Q

Which neurotransmitters does MAO A break down?

A

5-HT, NE, and Tryptamine

29
Q

Which neurotransmitters does MAO B break down?

A

Dopamine and Tryptamine

30
Q

In what cells are MAO A and MAO B?

A

All of them.

31
Q

Where is MAO within a cell?

A

On the outer mitochondrial membrane.

32
Q

Is MAO the only way to degrade neuroamines?

A

Nope, but don’t worry about the other degradation mechanisms.

33
Q

What breaks down monoamines in extra-neuronal sites?

A

Still MAO A and MAO B.

34
Q

What are 4 pharmacological mechanisms by which you can turn down the SNS?

A

Inhibit catecholamine synthesis.
Block vesicular transporters.
Block release.
Antagonize adrenergic receptors.

35
Q

What are 4 pharmacological mechanisms by which you can turn up the SNS?

A

Adrenergic agonists.
Promote release.
Inhibit reuptake.
Inhibit catabolism.

36
Q

Why don’t you inhibit the rate limiting step in catecholamine synthesis to turn down the SNS?

A

Because it’s not selective. If you inhibit tyrosine hydroxylase, you’ll knock down dopamine, NE, and epi.

37
Q

What does alpha-methyldopa do? What is it used for?

A

Inhibits LAAD.(which converts Dopa to Dopamine).

Hypertension - the MoA is weird, don’t worry about it.

38
Q

What does carbidopa do? What is it used for?

A

Inihbits LAAD just in the periphery.

Used in PD with L-dopa to make sure more L-dopa makes it to the CNS.

39
Q

What does tetraethylthiuram (disulfiram) do? What is it used for?

A

Inhibits dopamine beta-hydroxylase (which converts dopamine to NE).
Used for alcoholism - because it also inhibits acetylaldhyde dehydrogenase.
(more important for other lectures)

40
Q

What does reserpine do? What is it used for? Why is it a terrible drug?

A

Inhibits VMAT.
Used for hypertension (and snakebite!).
Causes big reduction in NE, epi (and some dopamine) -> profound drop in BP, and causes depression.

41
Q

What does bretylium do?
What is it used for?
Problem with it?

A

Blocks vesicular release of NE (after initially causing NE release).
Used for ventricular fibrillation.
It’s non-specific.

42
Q

What does guanethidine do?
What is it used for?
Problem with it?

A

Inhibits NE release.
It’s a powerful antihypertensive.
Leads to catecholamine depletion / nerve ending degradation.

43
Q

What two drugs block NE release?

A

Bretylium and guanethidine.

44
Q

What happens when you give someone dopamine? What is it used for?

A

Agonizes alpha and beta-1 adrenoreceptors in the periphery (doesn’t cross the BBB).
Used for management of shock, hypovolemia.
She notes that it’s “inotropic.”

45
Q

What does dobutamine do?

What is it used for?

A

Beta-1 adrenoreceptor agonist (more specific than dopamine).

Used in congestive heart failure.

46
Q

What does bromocriptine do?
What is it used for?
Trivia about it?

A

Selective D2 receptor agonist.
Used for Parkinson’s disease.
It’s an LSD derivative.

47
Q

What’s an important feature of amphetamine kinetics?

A

They resist MAO degradation.

48
Q

How do cocaine and tricyclic antidepressants work?

A

They inhibit reuptake.

49
Q

How does selegiline work?

What is it used for?

A

Inhibits MAO B (which breaks down dopamine and tryptamine) -maybe.
It’s used for PD (as adjunct) and as an antidepressant.
(despite us thinking that it acts on MAO B, it also appears to affect NE and 5-HTergic neurons)

50
Q

What are the 2 major systems for neurotransmitter reuptake? Briefly describe them. (Where? How fast? Capacity?)

A

Uptake 1: Uptake into nerve terminals. Fast (high affintiy), low capacity.
Uptake 2: Extra-neuronal uptake. Slow (low-affinity), high capacity.

51
Q

What does reserpine do? What is it used for? Why is it a terrible drug?

A

Inhibits VMAT.
Used for hypertension (and snakebite!).
Causes big reduction in NE, epi (and some dopamine) -> profound drop in BP, and causes depression.

Brain and Behavior Part 2 (58 decks)

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