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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
What does the appearance of MHPG​ in the cerebro-spinal fluid and urine indicate?
tells us the activity of CNS noradrenergic activity (30-50% of MHPG in the urine originates from the brain)
26
What is **VMA (vanillylmandelic acid)**? Where does it appear?
metabolite that is formed from metabolism of noradrenaline appears in peripheral neurons and the urine
27
What does the presence of VMA (vanillylmandelic acid) in the urine or peripheral neurons indicate?
peripheral sympathetic activity tumors * diagnostic- pheochromocytoma
28
How are catecholamines uptaken into **presynaptic terminals**?
active transport Na+ cotransport (Na, K ATPase) sustained depolarization * reverse function
29
What are **inhibitors** of the **uptake** of catecholamines by the presynaptic terminals?
cocain tricyclic antidepressants
30
What happens if the transporter does not capture all the released catecholamine to be taken into the presynaptic terminal?
diffusion from the nerve terminal to distant sites
31
Describe the specificity of the transporters that uptake catecholamines into presynaptic terminals.
specific for individual transmitters, but large homology between **noradrenaline** and **dopamine** transporters can transport certain psychostimulants that will enhance the effects of catecholamines
32
What effect does **α​ methyl- DOPA** have on **_DOPA- decarboxylase_**?
first: it is converted to α-methyl-noradrenaline it acts as a false transmitter and the effect is 1/10 of normal noradrenaline
33
What effect does **α-methyl-p-tyrosine** have on **_tyrosine hydroxylase_**?
competitive inhibitor of tyrosine enzyme cannot operate pheochromocytoma
34
What are the noradrenergic receptors?
35
How does noradrenergic innervation effect the heart and GI system? Via which receptor?
β1 ## Footnote **Heart**: + inotropic and chronotropic effect **GI system**: relaxation
36
How does hormonal stimulation (mainly by adrenaline) effect the uterus, striated muscle, and respiratory system? Via what receptor?
**β2** ## Footnote **uterus**: relaxation **striated muscle**: mobilization of glycogen **smooth muscle:** vasodilation **Respiratory System**: dilation
37
What is the affinity comparison between adrenaline and noradrenaline of β1 receptor?
**A** ≥ **NA**
38
What is the affinity comparison between adrenaline and noradrenaline of **β2 recepto**r?
**A** \> NA
39
What does the
40
What does the **β3 receptor** stimulate in adipose tissue?
lipolysis
41
Summary of physiological actions of adrenoceptor stimulation
42
What is the immediate action of β1 receptors in the heart?
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
What kind of Calcium channels are in the heart? What are they sensitive to?
**L-type Ca2+ channels** (long lasting) Sensitive to **DHP** and effects the α1 subunit
44
When can **DHP calcium channel blockers** be used?
in hypertension to decrease the blood pressure
45
What is the "late action" of β1 receptors in the heart?
Activation of sarcoplasmic reticulum Ca2+ ATPase ↓ Ca2+ goes back into SR
46
What is the function of **phospholambane** and when is it active?
active when DEphosphorylated **inhibits** SR Ca2+ ATPase (present only in heart)
47
What is the function of **cAMP-dependent protein** kinase activation?
phosphorylation of phospholambane (making it inactive) therefore SR **Ca2+ ATPase** is **activated** **↓** **relaxation** all together INCREASED HR
48
How can we treat arrhytmia?
β1 selective antagonists
49
What is angina?
decrease in the frequency of contractions
50
How is the β1 receptor stimulated in the heart?
Depolarization ↓ L-type Ca2+ channel (DHP receptor) activation ↓ Ca2+ entry ↓ Ca2+ induced Ca2+ release from SR ↓ **contraction**
51
What are substrates of **cAMP- dependent protein** kinase in the heart?
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
What is the effect of β1 and β3 receptors in adipose tissue?
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
What is the effect of **α1 receptors** on **adipose tissue**?
Ca2+ calmodulin * mobilization of glycogen * inhibitioin of glycogen synthesis
54
What is the effect of **α2 receptors** on **adipose tissue**?
cAMP ↓ * inhibition of lipolysis
55
Regulation of glycogen metabolism in **striatal muscle** scheme
56
Regulation of glycogen metabolism in **smooth muscle** scheme
57
What receptor is found in the **bronchi**?
β2
58
What receptor is found in the **intestinal smooth muscle**?
β1
59
What is receptor is found in the **uterus**?
β2
60
What receptor is found in **blood vessel walls**?
β2
61
What effects are mediated through the **α1 receptor**?
↑ glycogenolysis smooth muscle **contraction** in blood vessels
62
What effects are mediated through the **α2 receptor**?
intestinal smooth muscle **relaxation** **inhibition** of lipolysis platelet aggregation
63
What effects are mediated through the β1 receptor?
**stimulation** of lipolysis **↑** heart rate and force
64
What effects are mediated through the **β2 receptor**?
↑ glyconeogenesis ↑ glycogenolysis smooth muscle **relaxation** bronchi, blood vessels, intestine
65
Describe the series of events that occurr with the stimulation of the **α1** in the **liver.**
[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

Biochemistry III (8 decks)

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