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DRUGS > 4. Acetylcholine and co > Flashcards

4. Acetylcholine and co Flashcards

1
Q

acetylcholine synthesis

A

acetyl co A and choline by ChAT - choline acetyl transferase which is used for histological staining

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2
Q

acetylcholine breakdown

A

cholinesterases into constituents in synapse and then reuptaken

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3
Q

ACh CNS structures:

A 
magnocellular forebrain (nucleus basalis of meynertand septohippocampal pathway) and the brainstem (pedunculopontine  and laterodorsal tegmentum)
also striatal interneurons in rats but not humans (for movement)
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4
Q

what is ACh for?

A

attention and arousal

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5
Q

ACh CNS structures are

A

species dependent - rats ave striatal interneurons that we don’t have

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6
Q

Septohippocampal pathway

A

projects from the forebrain to the hippocampus - is important in short term memory and learning

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7
Q

NbM

A

Projects to the cotrex and also to the inhibitory layer of cells just above the thalamus - thalamic reticular nucleus - involved in general arousal

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8
Q

brain stem ACh

A

sleep wake cycles (cholinergic input –> thalamus = wake state) and motor activity

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9
Q

ACh receptors

A

nicotinic and muscarinic

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10
Q

Nicotinic ACh receptors

A

pentamers (homo or heteromeric) - fast EPSPs - Na/K or Ca permeability changes - move large hydrophobic residues out of channel pore and replace with small aqueous residues to form a pore lining - usually presynaptic to facilitate glutamate release

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11
Q

metabotropic ACh receptors

A

M1,3,5, - E (Change NA perm)
M2,4 - I (change K/Ca perm)
more widespread

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12
Q

Excitatory mAchRs

A

use the M current. wont generate an AP on their own but a small sustained current instead. If a stimulus is applied during the M current it’ll fire a train of action potentials. it synaptic sensitivity.

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13
Q

Histamine synthesis

A

synthesise from histadine by histadine decarboxylase (only 64000 cells)

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14
Q

histamine metabolism

A

broken down by histmaine methyltransferase to methylhistamine and the broken down by MAO

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15
Q

histamine projects to

A

thalamus!! cortex, amygdala, hypothalamus - the system is more developed in lower mammals - switch on and off in wake and sleep state (discrete)

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16
Q

histamine in the body

A

stimulates release of bradykinin in response to damage

17
Q

H1

A

cAMP (E)

7TMDs GPCR

18
Q

H2

A

IP3 (E)

7TMDs GPCR

19
Q

H3

A

auto/heterocetor?

7TMDs GPCR

20
Q

histamine drugs: H1

A

Old ones used to be sedative but new ones can’t cross BBB - treat allergies and stings

21
Q

histamine drugs: H2

A

used to treat acidity and stomach ulcers - BBB impermeable

22
Q

histamine drugs: H3

A

analogues used to treat chronic dizziness in the vestibular system

23
Q

Neuropeptides SYNTHESIS

A

Always in the soma but can be transported to the terminal as a co-molecule or in its active form

24
Q

Neuropeptides NT’S?

A

vesicualr release, ca dependent, act on GPCRs but no obvious fast actions - only slow modulatory effects
but co transmission

25
Q

co-transmission

A

neuropeptides released alongside other NTs to extend their maximal effects
(e.g. salivary glands, VIP only released at high freq. firing to extend ACh action)
However some places have NTs as primary form of transmission

26
Q

Purines

A

e.g. adenosine (ATP) can be released (free of vesicles) as a soup to act on A1/2/2B/3 - more protective than transmissive - prevents hyperexcitability - acts on same system as caffeine. produced de novo.

27
Q

Melatonin

A

produced in the pineal gland fro serotonin - acts on MT1/2 in the retina and brain - synthesis stimulated by night and day- used to treat depression, ADHD and jetlag

28
Q

NO

A

Nitric oxide is produced in response to elevates ca levels (de novo) by NOS (NO synthase) and released paracrinally - effecting cells up to 400um away - it can have both inhibitory and excitatory effects (seconds to minutes)

29
Q

roles of NO

A

co transmitter in PPT pathway of ACh. LTP and neurotoxicity (from excitabiity)

30
Q

name the lipid transmitters:

A

endocannabinoids (2AG and anadamide) Eicosanoids, protsalglandins and leukotrienes.

31
Q

lipid NT transmission and synthesis:

A

retrograde transmission both auto and paracrinally. They can modulate glutamate and gaba release. Cell signalled and arachadonic acid formed from part of the membrane. this converted into EC/Ei which are then released to act on presynaptic cells.

32
Q

EC receptors

A

CB1/2 are used in the treatment of pain and nausea. they can alter both glutamate and gaba release through retrograde signalling

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