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Biochemistry III > Noradrenergic Neurotransmission > Flashcards

Noradrenergic Neurotransmission Flashcards

1
Q

What are cathecholamines synthesized from?

A

tyrosine

structure: cathecol plus amine containing side chain

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2
Q

What is noradrenaline- norepinephrine and where can it be found?

A

neurotransmitter

  • brain
  • postganglionic sympathetic neurons
  • small amount in the circulation as hormone
  • CNS and autonomic nervous system
  • adrenal medulla
    • only small portion of cells (N cells) release noradrenaline
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3
Q

What is adrenaline- epinephrine and where can it be found?

A

hormone

  • adrenal medulla
    • most of the cells (A cells) release adrenaline
  • in small portion of neurons in the central nervous system (in the brain)
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4
Q

What is dopamine and where can it be found?

A

neurotransmitter

  • brain
  • modulator- in the periphery (kidney)
  • CNS
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5
Q

What areas of the body recieve noradrenergic innervation?

A
  1. Central Nervous system
  2. Postganglionic sympathetic neurons
    • heart
    • intestinal smooth muscle
    • blood vessels
    • bronchi
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6
Q

Where is norepinephrine synthesized?

A

locus coeruleus

tegmentum

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7
Q

What is the rate limiting enzyme in the biosynthesis of noradrenaline?

A

tyrosine hydroxylase

  • negative feed-back inhibition by noradrenaline
  • activation by Ca2+
  • phosphorylation by PKA, PKC, and Ca 2+ / calmodulin-dependent kinase
    • increases the affinity for the pterin cofactor
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8
Q

How is the activity of tyrosine hydroxylase effected by an increase in sympathetic activity?

A

increased tyrosine hydroxylase activity

  • no negative feedback inhibition
  • Ca2+ entry into nerve terminals
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9
Q

What happens to tyrosine hydroxylase in the event of long term activity?

A

the amount of the enzyme is increased

( dopamin b-hydroxylase level is also elevated)

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10
Q

What is the effect of steroid hormones on the synthesis of noradrenaline?

A

increase the activity of N-methyltransferase

⇒ increased synthesis of adrenalin

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11
Q

In therapy what is used for the treatment of hypertension?

A

α-metil-DOPA

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12
Q

In therapy what is used for the treatment of Parkinson’s disease?

A

L-DOPA

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13
Q

How is norepinphrine/epinephrine/dopamine uptaken into synaptic vesicles?

A

VMTA 2

vesicular membrane transporter 2

* may have altered expression in bipolar disease *

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14
Q

Describe the specificity of VMAT 2?

A

broad substrate-specificity to biogenic amines

(tripatmine, tiramine, amfetamin- compete with endogenous catecholamines)

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15
Q

What is reserpine?

A

high affinity irreversible inhibitor of VMAT 2

effects storage

NA depletion

* depletion of vesicles *

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16
Q

What enzymes are responsible for the metabolism of noradrenaline?

A

MAO

COMT

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17
Q

What is the method of which MAO metabolizes noradrenaline?

A

oxidative deamination of cetacholamines

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18
Q

What is the method of which COMT metabolizes noradrenaline?

A

methyl transfer to the 3-hyrdoxy group on the ring from S-adenosylmethionine

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19
Q

Where is MAO located?

A
  • widely distributed throughout the body
    • locates on the outer membrane of the mitochondria
  • intraneuronal + (some in the synapse- MAO B)
    • cell body
    • axon terminal
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20
Q

What are the different isoenzymes of MAO?

A

* different substrate specificity and inhibitors *

MAO A

  • preference to noradrenaline and serotonin

MAO B

  • synthetic substrates
  • Dopamine
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21
Q

What is an inhibitor of MAO?

A

Clorgilin

Deprenyl (Parkinsons disease)

Selegylin

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22
Q

What is the function of MAO in the gastrointestinal tract or liver?

A

prevents accesss of ingested indirectly acting amines (tyramine, phenylethylamine) to the general circulation

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23
Q

Where is COMT located?

A

intra and extraneuronal

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24
Q

What is the main metabolite produced from the metabolism of noradrenaline in the brain? Where does it appear?

A

MHPG​

cerebro-spinal fluid and urine

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25
Q

What does the appearance of MHPG​ in the cerebro-spinal fluid and urine indicate?

A

tells us the activity of CNS noradrenergic activity

(30-50% of MHPG in the urine originates from the brain)

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26
Q

What is VMA (vanillylmandelic acid)? Where does it appear?

A

metabolite that is formed from metabolism of noradrenaline

appears in peripheral neurons and the urine

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27
Q

What does the presence of VMA (vanillylmandelic acid) in the urine or peripheral neurons indicate?

A

peripheral sympathetic activity

tumors

  • diagnostic- pheochromocytoma
28
Q

How are catecholamines uptaken into presynaptic terminals?

A

active transport

Na+ cotransport (Na, K ATPase)

sustained depolarization

  • reverse function
29
Q

What are inhibitors of the uptake of catecholamines by the presynaptic terminals?

A

cocain

tricyclic antidepressants

30
Q

What happens if the transporter does not capture all the released catecholamine to be taken into the presynaptic terminal?

A

diffusion from the nerve terminal to distant sites

31
Q

Describe the specificity of the transporters that uptake catecholamines into presynaptic terminals.

A

specific for individual transmitters, but large homology between noradrenaline and dopamine transporters

can transport certain psychostimulants that will enhance the effects of catecholamines

32
Q

What effect does α​ methyl- DOPA have on DOPA- decarboxylase?

A

first: it is converted to α-methyl-noradrenaline

it acts as a false transmitter and the effect is 1/10 of normal noradrenaline

33
Q

What effect does α-methyl-p-tyrosine have on tyrosine hydroxylase?

A

competitive inhibitor of tyrosine

enzyme cannot operate

pheochromocytoma

34
Q

What are the noradrenergic receptors?

A
35
Q

How does noradrenergic innervation effect the heart and GI system? Via which receptor?

A

β1

Heart: + inotropic and chronotropic effect

GI system: relaxation

36
Q

How does hormonal stimulation (mainly by adrenaline) effect the uterus, striated muscle, and respiratory system? Via what receptor?

A

β2

uterus: relaxation

striated muscle: mobilization of glycogen

smooth muscle: vasodilation

Respiratory System: dilation

37
Q

What is the affinity comparison between adrenaline and noradrenaline of β1 receptor?

A

A ≥ NA

38
Q

What is the affinity comparison between adrenaline and noradrenaline of β2 receptor?

A

A > NA

39
Q

What does the

A
40
Q

What does the β3 receptor stimulate in adipose tissue?

A

lipolysis

41
Q

Summary of physiological actions of adrenoceptor stimulation

A
42
Q

What is the immediate action of β1 receptors in the heart?

A

cAMP-dependent protein kinase

↓

phosphorylation of plasma membrane Ca2+ channels

↓

Ca2+ entry → Ca2+ induced Ca2+ release from the SR

↓

Rise in intracellular [Ca2+]

↓

increased force of contraction

+ inotropic effect

43
Q

What kind of Calcium channels are in the heart? What are they sensitive to?

A

L-type Ca2+ channels

(long lasting)

Sensitive to DHP and effects the α1 subunit

44
Q

When can DHP calcium channel blockers be used?

A

in hypertension to decrease the blood pressure

45
Q

What is the “late action” of β1 receptors in the heart?

A

Activation of sarcoplasmic reticulum Ca2+ ATPase

↓

Ca2+ goes back into SR

46
Q

What is the function of phospholambane and when is it active?

A

active when DEphosphorylated

inhibits SR Ca2+ ATPase

(present only in heart)

47
Q

What is the function of cAMP-dependent protein kinase activation?

A

phosphorylation of phospholambane

(making it inactive)

therefore SR Ca2+ ATPase is activated

↓

relaxation

all together INCREASED HR

48
Q

How can we treat arrhytmia?

A

β1 selective antagonists

49
Q

What is angina?

A

decrease in the frequency of contractions

50
Q

How is the β1 receptor stimulated in the heart?

A

Depolarization

↓

L-type Ca2+ channel (DHP receptor) activation

↓

Ca2+ entry

↓

Ca2+ induced Ca2+ release from SR

↓

contraction

51
Q

What are substrates of cAMP- dependent protein kinase in the heart?

A
  1. Plasma membrane L- Ca2+ channels

↑ release of Ca 2+ from SR by Ca2+ induced Ca2+ release

* positive inotropic effect *

2. Phospholambane

↑ Ca2+ return to SR

* positive chronotropic effect*

​

​

52
Q

What is the effect of β1 and β3 receptors in adipose tissue?

A

cAMP ↑

↓

cAMP dependent protein kinase

↓

a. ) hormone sensitive lipase → lipolysis
b. ) Glycogen phosphorylase kinase → mobilization of glycogen
c. ) Glycogen synthase → inhibition of glycogen synthesis

53
Q

What is the effect of α1 receptors on adipose tissue?

A

Ca2+ calmodulin

  • mobilization of glycogen
  • inhibitioin of glycogen synthesis
54
Q

What is the effect of α2 receptors on adipose tissue?

A

cAMP ↓

  • inhibition of lipolysis
55
Q

Regulation of glycogen metabolism in striatal muscle scheme

A
56
Q

Regulation of glycogen metabolism in smooth muscle scheme

A
57
Q

What receptor is found in the bronchi?

A

β2

58
Q

What receptor is found in the intestinal smooth muscle?

A

β1

59
Q

What is receptor is found in the uterus?

A

β2

60
Q

What receptor is found in blood vessel walls?

A

β2

61
Q

What effects are mediated through the α1 receptor?

A

↑ glycogenolysis

smooth muscle contraction in blood vessels

62
Q

What effects are mediated through the α2 receptor?

A

intestinal smooth muscle relaxation

inhibition of lipolysis

platelet aggregation

63
Q

What effects are mediated through the β1 receptor?

A

stimulation of lipolysis

↑ heart rate and force

64
Q

What effects are mediated through the β2 receptor?

A

↑ glyconeogenesis

↑ glycogenolysis

smooth muscle relaxation

bronchi, blood vessels, intestine

65
Q

Describe the series of events that occurr with the stimulation of the α1 in the liver.

A

[Ca2+]i ↑

↓

Ca2+ -CAM complex

↓

Activation of glycogen phosphorylase kinase

↓

glycogen breakdown

↓

Glu-1-P → GLU-6-P → GLU

↓

RISE in blood glucose level

66
Q
A

Biochemistry III (8 decks)

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