Neuropharmacology Flashcards

(71 cards)

1
Q

ACh

A

choline + acetyl CoA - choline acetyl transferase (CAT) -> ACh (synapse, neuromuscular junction or effector tissue) -> acetyl choline esterase AChE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Muscarinic receptors mAChR

A

g protein, parasympathetic (target tissues), CNS modulation (memory = Alzheimers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

M1, M3

A

gastric function and salivary + stomach secretion via Ca (+M5 activate Gaq (Ca)) (M3= vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

M2

A

reduce heart rate and neuronal excitability (+ M4 inhibit Gai/o, presynapse and post)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Nicotinic receptors nAChR

A

sympathetic (indirectly-ganglion) parasympathetic, sodium channels (memory, cognition = ADHD, schizophrenia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acetylcholinesterase AChE

A

-> choline and acetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

NE

A

neurotransmitter, selective for alpha - phenylalanine, tyrosine, dopamine -> NE -> monoamine oxidase (arousal, attention, memory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Adrenaline

A

hormone, selective for beta - phenylalanine -> l dopa -> dopamine -> NA -> A, locus coerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

NET

A

Noradrenaline transporter, DAT - dopamine = reuptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

a1 adrenoreceptor

A

Gq, Ca2+, vasoconstriction (skin and GI tract)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

a2 adrenoreceptor

A

Gi, brain, reduce presynaptic neuron NA release (modulation) via ions?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

B1 adrenoreceptor

A

Gs, Ca2+, cardiac output and renal, CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

B2 adrenoreceptor

A

Gs , v K+=hyperpolarisation, bronchodilation, vasodilation (muscular), gluconeogenesis, GI motility, CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

B3 adrenoreceptor

A

Gs, adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Glutamate

A

glutamine via glutaminase, taken up by astrocytes (EAAT1/EAAT2 transporters), main excitatory neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Group 1 metabotropic glutamate receptor

A

post synaptic, GqmGlu1 and 5, long term depression too much = bad, not enough =decrease brain activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Group 2 metabotropic glutamate receptor

A

presynaptic, GimGlu2, 3 - prevents release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Group 3 metabotropic glutamate receptor

A

presynaptic, GimGlu 4, 6, 7, 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

AMPA ion channel glutamate receptor

A

Na, most common, activated NMDA, increase with Na2+ (LTP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Kainate ion channel glutamate receptor

A

Na, post (excitatory), pre (net inhibitory via GABA increasing), hippocampus (memory and learning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

NMDA ion channel glutamate receptor

A

Na+Ca, LTP, both glutamate and glycine, Mg blocks, depression and schizophrenia,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

LTP

A

long term potentiation (learning), synaptic plasticity, strengthen connection =fire at low threshold stimulus (hippocampus, amygdala), associative/specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Excitotoxicity

A

too much Ca kills neurons, epilepsy - ALS disease (EAAT2), ischemic stroke (no oxygen = no ATP = depolarisation, Glutamate = neuronal cell death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

NE a1 agonist

A

Phenylephrine = vasoconstriction, nasal decongestant, acute hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
NE a2 agonist
Clonidine- (reduce NA release) = hypertension (reduce sympathetic activity), anxiety, migraine and to produce sedation
26
NE B blocker
Propranolol = anxiety, migraines, CV disease
27
NE B2 agonist
Salbutamol = asthma (relief inhalers), cause bronchodilation (salmeterol long term)
28
NE B1 antagonist
Atenolol, metoprolol = cardiovascular disease, including tachycardia and arrhythmias, block symp
29
NET/DAT inhibitor
ADHD Methylphenidate (NET/DAT) and atomoxetine (NET) - inhibits reuptake
30
Amphetamine
ADHD facilitate release of NA and dopamine via binding to vesicle storage proteins and transporters
31
a2 agonists used in ADHD
Guanfacine and clonidine - lowers bp
32
MDMA
dopamine facilitated release
33
AMPA positive allosteric modulator
Ampakines -noontropics, reduce AMPA agonist side effects, stimulate LTP (Recetams)
34
red algae
Kainic acid, domoic = toxic - too much stimulation, neurons all fire together, confusion, memory loss
35
NMDA competitive antagonists
Ketamine - anaesthetic, amnesia, antidepressant (low dose) | PCP - schizophrenic symptoms, temp decrease memory and learning
36
NMDA - non competitive antagonist
Memantine - Alzheimer's (neuroprotection from excitotoxicity)
37
GABA
glutamate via glutamic acid decarboxylase (GAD), GAT - recycling, GABA transaminase= breakdown, main inhibitory
38
GABAa +c
ionotropic, Cl+ transport, pentameric (binding a+B),
39
GABAb
GiPCR, post- inhibits adenylyl cyclase -> activates GIRK (K+ out of cell), pre-blocks Ca2+
40
GABAergic drugs
anxiety, depression, general anaesthesia, muscle spasms
41
Low expression of GABAa
impulse control, motivation, increase drug taking (low a2 subunit expression)
42
Drug similar to GABA
Gabapentin - doesn't bind to GABAa, increase GAD, decrease VGCC and glutamate (NMDAr), pain + migraines - anti-epileptic
43
covalent (suicide) inhibitor for GABA transaminase
Vigobotrin (side effects = drowsiness, dizziness, fatigue) - anti-epileptic
44
positive allosteric modulator GABAa
Benzodiazepines (diazepam) - a&y, sedative, hard to quit, reduce anxiety
45
Z-drugs
(zopiclone) - sleeping, a&y, (side effects= driving, tolerance, hallucinations)
46
GABAb activator
Baclofen - muscle spasms (epilepsy)
47
Dopamine
L-tyrosine, L-DOPA->. Breadown via monoamine oxidase. Ventral tegmental area + substantia nigria ->stiatum + nuclear accumbens + motor cortex.
48
D1
GsPCRs (post)
49
D2
GiPCRs (post and pre)
50
reward pathway
VTA -> Nucleus accumbens (regulated by hippocampus), schizophrenia=overstimulation (+ve -increase consciousness-salience, prefrontal cortex, -ve - not social)
51
Parkinsons
Substantia vigria -> striatum (low level of dopamine via pe cell death, tremor, bradykinesia)
52
Hypoglutamate hypothesis
glutamate in VTA stimulates dopamine neurotransmission to PFC and nucleus accumbus (ketamine and PCP help schizophrenia symptoms)
53
Parkinsons precursor
L-dopa +carbidopa (DOPA decarboxylase inhibitor), dopamine produces and used when needed (high dose = dyskinesia, muscle contraction, hallucinations, change therapeutic index)
54
Parkinsons treatment
increase dopamine in corpus striatum
55
dopamine receptor agonist examples
Bromocriptine (oral) + apomorphine (subcutaneous) - (hallucinations, vomiting, disruption of reward pathway-gambling, impulsive) - Parkinson's
56
MAOb inhibitor
Selegiline - decrease breakdown dopamine + NA, depression, in combination with L-dopa
57
D2 antagonist schizophrenia
Haloperidol - typical antipsychotics, non selective= a1-hypotension+dizziness, H1-sedation, weight gain, mAChR-reduce parasympathetic. (Parkinson's symptoms, lack of pleasure anhedonia)
58
D1 and D2 inhibitor schizophrenia
Clozapine - also serotonin receptors, increase dopamine-negative symptoms, less side effects
59
Seretonin
5-HT made from tryptophan, broken down by MAOa, SERT uptake, 10% brain=mood, sleep, reality perception, daydreaming (default mode network), 90% GI tract
60
Serotonin receptors
7 subtypes Gi, Gq, Na+ and Gs.
61
Depression
moamine theory=decrease in monoamine neurotransmission->less post synaptic activation (lack of serotonin doesn’t cause depression+placebo effect)
62
SSRI
selective seretonin reuptake inhibitors, selectively increase serotonin, first-line, low side effects (dry mouth, insomnia, nausea)
63
Tricyclic antidepressants SNRIs
NAT +SERT inhibitors, side effects- a1, H1, mAChR, overdose danger
64
Monoamine oxidase inhibitor effects
first created, irreversible or reversible, narrow therapeutic index, don’t metablise marmite, cheese, beer -> increase NE (last line)
65
Seretonin syndrome
MOAIs with SSRIs, TCAs or MDMA=synergetic toxicity-> delirium
66
Anxiety
psychological + physiological, increase heart rate, tremor, independent of external events (GAD, panic, phobia, PTSD, OCD)
67
SSRI example
Fluoxetine (used in depression and anxiety at lower dose)
68
Tricyclic antidepressant examples
Amitriptyline and nortriptyline
69
MAO inhibitor examples
Moclobemide - MAOa (NA+S), Selegeline - MAOb (NA+D), Phenelzine - non selective inhibitors
70
Ketamine in depression
treatment resistant depression, disinhibits GABAergic interneurons, blocks GABA release -> dopamine in hippocampus/VTA
71
Anxiety drugs
Propranolol and clonidine/guanfacine - NE modulators, prop reduce heart rate, clon decrease NE. Benzodiazepines