NT metabolism Flashcards

1
Q

A purinergic synapse is made up of two molecules

A

ATP and adensoine

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2
Q

Receptors of ATP

A

P2Y and P2X

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3
Q

Which enzyme is responsible for the hydrolysis of ATP into Adesnosine

A

ectodiphosphohydrolase/ ecto 5’ nucleotidsse

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4
Q

example of 1 datty acid and phosphate molecule

A

phosphotidylserine

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5
Q

Define lipid raft

A

cholesterol rich patches of cell membrane forming a distinct microenvironment that can cluster receptors for faster dimmerization eg FGF receptors

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6
Q
Name the cholesterol derivatives form
THC
Prostaglandin
Anandamide
Cholesterol
A

Cortisol
estradiol
testosterone
Vitamin D3

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7
Q

How does endocannabinoid signalling work?

A

Endocannabinoids are synthesized upon demand. trigger signal : calcium elevation or mGluR activation. ECs act as retrograde messengers, suppressing presynaptic release of inhibitory NTs

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8
Q

Arachidonic acid annd glycerol lead to

A

acetylCoA

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9
Q

Purinergic receptors for
adenosine
ATP, UTP

A

P1 gprotein coupled

P2x ligand gated and P2Y G protein coupled

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10
Q

How is anandamide metabolised

A

Degenerated by Fatty Acid amide hydrolase to arachidonic acid and ethanolamine

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11
Q

Otto loewi’s experiment on vagusstoff was which NT

A

ACh

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12
Q

What is depolarization induced supression of inhibition

A

when endocannabinoids are activated by calcium elevvation or activation of metabotropic glutamate receptors, depolarization induced supression of inhibition occurs. Ca and mGluR act as retrograde messengers to supress synaptic release

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13
Q
Classify the NTs
Glutamine, GABA, Glycine
ACh, NE, DA, Histamine 5HT
Substance P, enkephalins, somatostatin, neuropeptide Y
2AG, anandamide
A

Glutamine, GABA, Glycine- amino acids
ACh, NE, DA, Histamine 5HT-amines
Substance P, enkephalins, somatostatin, NEUROPEPTIDE y-peptides
2AG, anandamide- endocannabinoids

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14
Q

In vesicular transport glutamate and GABA depend on which gradients?

A

Glutamate is -vely charged, makes it easier to exchange a H+, electrochemical gradient greater than pH gradient
GABA depends on both pH and electro because it’s a Zwitter ion
ACh is +vely charged, more on pH than electrochemical

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15
Q

Role of AISIC channels in the hippocampus interneurons

A

They are activated by protons, hence activate inhibition if excitation, causing termination of seizures,Low pH mediates a cationic current, leading to depolarization

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16
Q

Consequence of impaired acidification

A

Decreased amplitude in the post synapse hence cortical spread in depolarization

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17
Q

2 ways of glutamate synthesis

A

Glutamine (PAG)-glutamic acid-(decarboxylase)GABA-

alphaketoglutarate through glu-aminotransferase to glutamate

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18
Q

Energy of vGlut transporter provided by

A

electrochemical gradient more than pH gradient

19
Q

Name 2 EAAT transporters and what is the main gradient

A

EAAT is a PM transporter for clearance. Uses sodium gradient, counter transports potassium. Transports glutamate and cleaves it, fast binding to Glu to reduce Glu transiently.
EAAT1 and 2-glia main glu transporter in hippocampus
EAAT 3-neurons

20
Q

recycling of glutamate

A

Glutamine synthetase in astrocytes converts glutamate to glutamine. Glu is excitatory so only glutamine will be taken up by astrocytes because it’s not neuroactive. Then at presynapse, glutamine is converted to glutamate by glutaminase

21
Q

Loading of GABA vesicles is by

A

vGAT, which has low substrate affinity

22
Q

Transport of GABA and glycine is by

A

VIAAT. using a proton gradient produced by vesicular ATPase/

23
Q

Generation of GABA

A

alpha ketoglutarate-GABAT-glutamate-Glutamic acid decarboxylase-Gamma ammino butyric acid

24
Q

Role of GAT 1

A

GAT-1 regulates tonic GABA-R mediated inhibition. Inactivates GABA for reuptake by the pre-synapse

25
Q

GHB is

A

Gamma hydroxybutiric acid, derivative of GABA, GABA B receptor agonist

26
Q

How is glycine cleared from the synaptic cleft

A

GLY T1 and GLY2 remove glycine from the synaptic cleft

27
Q

How is glycine produced

A

from serine via serin hydroxymethyltransferase at the MT

28
Q

How is acetylcholine generated?

A

Acetylcoenzyme A+choline via choline acetyltransferase

29
Q

How is acetylcholine broken down into choline and acetate

A

acetylcholine esterase inactivates ACh

30
Q

Between vACht and Vmonoamine transporters, which one has greater velocity?

A

VMATs have greater velocity and higher binding affinity becasue of substrate cytotoxicity

31
Q

How are ACh vesicles loaded?

A

Via vesicular ACh transporter which has a higher pH gradient compared to electrochemical gradient because ACh is +vely charged. vACh has low binding affinity and is slow due to high intracellular conc of ACh.

32
Q

Drugs that interfere with ACh

A

vesamicol inhibits vACH transporter
Curare and mecamylamine are nicotinic antagonist blocks, block nicotinic ACh receptors
Botulinus and Tetanus- inhibit ACh release (vesicular release and docking)
Spider toxin stimulates release

33
Q

Name 2 muscarinic agonists

A

atropine

benzatropine

34
Q

2 mechanisms of ACh inactivation mechanims

A

diffusion out of cleft

Acetylcholinesterase enzymatic degradation

35
Q

True/false. Nicotinergic/ionergic transmission is rare in CNS

A

True. More nicotinic receprors in muscular endplate

36
Q

DA, NE and epinephrine are exmples of

A

catecholamines

37
Q

seratonin is derived from which aa

A

tryptophan

38
Q

how is DA derived

A

L-tyrosine- tyrosine hydroxylase-L-DOPA-DOPA decarboxylase-Dopamine

39
Q

how is norepinephrine derived

A

dopamine-dopamine hydroxylase-NE-Nmethyltransferase-Epinephrine

40
Q

Catecholamine vesicular transporter

A

vesicular monoamine transporter VMAT, Mg dependent

41
Q

Neuronal catecholamine transporter

A

DA transporter

NE transporter use sodium /potassium ATPase

42
Q

Inactivation of catecholamines

A

monoamine oxidase, catechol-0-methyltransferase

43
Q

Most antipsychotic drugs block which receptors of DA

A

D2

44
Q

Seratonin production

A

tryptophan- tryptophan hydroxylase- 5HTP-l aromatic acid decarboxylase- 5HT/seratonin