W3 Flipped lecture content Flashcards

1
Q

Acetylcholine acts on what?

A

Nicotinic (iontropic and muscarinic metabotropic) receptors.

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2
Q

Acetycholine

A

created by combined acetyl and choline. Acetylcholine Destroyed in the synaptic cleft by an enzyme. Choline is recycled to make more acetylcholine.

ChAT = good marker for cholinergic neurons.
Acetyl CoA

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3
Q

Nicotinic (nAChRs):

A

ACh-gated Na+/Ca2+ channel, found at neuromuscular junction, CNS.

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4
Q

Muscarinic (mAChRs)

A

5 types of GPCRs, found in CNS and autonomic nervous system. Recall Loewi’s 1921 experiment on the heart: the ‘vagusstoff’ was ACh!

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5
Q

Neutroasmitter at the neuromyscluar junction (NMJ)

A

Acetylcholine used as a neuromusclar hunction, NMJ motor nerve excites the muscle.

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6
Q
  1. Block release [Acetylcholine: pharmacology]
A
  1. Block release (paralyzing you).

Botulinum towin (produced by bacteria),

Black widow spier venom (first increases ACh release at NMJ then elminates it. Seems to work by allowing a big calcium influx)

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7
Q

Acetylcholine: pharmacology

A
  1. Block release
  2. Block AchE
  3. Activate ACh Receptors
  4. Block ACh receptors
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8
Q

Block AchE [Acetylcholine: pharmacology]

A

Nerve gas
Organophosphate pesticides
Alzheimer’s treatments

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9
Q
  1. Activate ACh receptors [Acetylcholine: pharmacology]
A

Nicotine, muscarine
Neonicotinoid pesticides

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10
Q

Block ACh receptors [Acetylcholine: pharmacology]

A

Nicotinic (curare)
Alpha bungarotoxin from snake venom binds to nAChRs and takes days to unbind
Bungarus multicinctus, alpha-bngarotoxin
Muscarinic: atropine

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11
Q

Monoamines are synthesised from what?

A

Amino acids.

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12
Q

Epinephrine

A

Adrenaline, named after the adrenal gland

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13
Q

Storage adn removal of monamines

A

Pached into vesicles by vesicular monoamine transporters (VMAT)
Removed from the synaptic cleft by re-uptake transporters
Destroyed by monoamine oxidase (MAO) and catechol-O-methyltransferase

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14
Q

What are the epinephrine, norepinephrine receptors

A

Adrenergic recpeotrs; alpha and beta types

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15
Q

Different receptors

A

activate different Gprotein effectors. Different receptors are expressed in different neuron types or parts of the brain. That’s why drugs can have specific effects.

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16
Q

Dopamine Motor control

A

Dopaminergic neurons in the substantia nigra prokect to the striatum. This nigrostriatal pathway facilitations initiation of voluntary movement. These neurons die in PD = motor dysfunction

17
Q

How can PD be trated

A

Increasing dopamine.
TH is rate-limiting in synthesis of dopamine, so can give L-DOPA (dopamine doesn’t cross the blood-brain barrier
The loss of the dopaminergic neurons causes the motor symptoms.D

18
Q

Dopamine - Reward

A

Dopaminergic neurons in the ventral tegmental area (VTA) prokect to the cortex and limbic system. This mesolimbic pathway mediates ‘reawrd’/’motivation’

19
Q

Cocaine, amphetamines

A

Block reuptake of dopamine, norepinehrine

20
Q

Antipsychotics

A

Block dopamine receptors (parkinson’s like symptoms (possible side effect))

21
Q

Antidepresents

A

-tricyclics: block reuptake of NE, serotonin
-selective serotonin reuptake inhibitors (SSRIs), e.g. fluoxetine (Prozac)
-MAO-A inhibitors

22
Q

Opinoid peptides (endorphins)

A

Bind to opioid receptors (GPCRs)
Regulate pain (perception/emotion/cognitive)
Also regulate coughing, GI tract.
Opioid receptors are the targets of morphine, heroin.

23
Q

ATP

A

often a co-transmitter

24
Q

Nitric Oxide

A

Gas, membrane-permeable
Acts on soluble guanylate cyclase, not a membrane receptor

25
Q

Endocannabinoids

A

Lipid-soluble, not in vesicles
Ca2+ triggers synthesis, not vesicle fusion
Retrograde signaling (postpre)
Bind to GPCRs (the targets of the active compound in cannabis)