Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neuropharmacology > Cannabis - endocannabinoids and G proteins > Flashcards

Cannabis - endocannabinoids and G proteins Flashcards

(57 cards)

Start Studying
1
Q

uses of cannabis

A

industrial - hemp
religious rituals
recreational use

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

recreational use of cannabis §

A

smoked or injested
widely used but usage going down
(dried flowers, resin or liquid extracts)

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

types of effects of cannabis

A

psychotropic (mainly)

somatic

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

psychotropic effects of cannabis

A 
change in perception
euphoria 
increase in appetite
relaxation 
increased appreciation of music 
Introspection
enhanced episodic memory
increased awareness of sensation

At higher doses
auditory and/or visual illusions
hallucinations
ataxia

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

euphoria

A

heightened mood

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

episodic memory

A

recollection

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

ataxia

A

lack of voluntary control of muscle movement

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

somatic effects of cannabis

A 
increased HR
dry mouth
reddening of the eyes
reduction in intra-ocular pressure 
muscle relaxation
Electroencephalography or EEG: more persistent alpha waves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cannabis used to treat glaucoma due to

A

its ability to reduce intra-ocular pressure

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

how can cannabis be used in treatment of bronchial asthma

A

cannabis causes bronchial dilation

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

how can the antiemetic effect of cannabis be used as a therapeutic

A

treats the nausea/vomiting caused by anti cancer drugs

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

other therapeutic uses of cannabis

A

apetite stimulant
analgesia
ataxia - to treat muscular sclerosis etc

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

mental health risks of cannabis

A 
Triggering psychotic episodes and psychosis
Increase risk of schizophrenia
Anxiety
Paranoia
Substance abuse disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

physical health risks of cannabis

A 
Lung problems (due to ingestion by smoking)
Lung cancer (cannabis often combined with tobacco)
Increased heart rate/blood pressure --> heart problems
Foetal developmental (if consumed when pregnant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

legal/societal risks

A

prison sentence
fine
criminal record

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

how many cannabinoids found in recreational cannabis

A

66

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

example of cannabinoids found in cannabis

A

delta9-tetrahydrocannabinol

cannabinol

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

2 canonical cannabinoid receptors

A

CB1
CB2

known about for ages

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

other possible non-canonical cannabinoid receptors

A

GPR55
GPR119
GPR18

recently discovered

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

CB1 receptor expression

A

mainly in the brain, kidneys, liver and lungs

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

CB2 receptor expression

A

immune cells and macrophages

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

which cannabinoid receptor is a potential therapeutic target

A

CB2

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

structure of CB1 receptor

Study These Flashcards
A

7 transmembrane domain
extracellular N terminal binds to agonist
intracelular C terminal associated with downstream signalling

24
Q

when ligand eg THC binds to CB1 receptor

Study These Flashcards
A

moves from resting state (Ga bound to GDP)
conformational change
GTP then binds to Ga
Ga dissociates from GB/y complex

25
which G protein subunits are CB1 receptors coupled to
Gi/o
26
what happens when Gai/o dissociates from GB/y
Gai/o: - shuts Ca2+ channels into the cell - inhibits adenyl cyclase --> decreased cAMP GB/y: - positively regulates GIRK channels --> increased K+
27
CB1 receptor location
ubiquitous across the brain but more densely located in higher functioning areas e.g. neocortex, hippocampus presynaptic
28
use of binding assays
tell us how well the radioactive ligand binds to its receptor
29
assays for measuring receptor pharmacology
binding assays | functional assays
30
use of functional assay
determines how activated the receptor is | measure EC50
31
Ki
binding affinity | constant
32
Ki of THC
10-50nM
33
why does THC have a low efficacy
it is a partial agonist | compared to synthetic ligands
34
features of synthetic ligands
much higher efficacy and potency
35
effect of cannabidiol at CB1 receptors
functional antagonist | shifts the curve to the right (concentration-response curve)
36
role of CB1 receptors at synapses
modulate inhibitory synaptic transmission
37
effect of CB1 agonists
inhibit GABA-mediated synaptic transmission
38
possible post synaptic mechanism of CB1 R agonist
reduce postsynaptic sensitivity to GABA
39
possible pre synaptic mechanism of CB1 R agonist
reduce presynaptic release probability
40
each quantal release
corresponds to each miniature IPSC
41
If amplitude of events reduced ...
then the neurotransmitter has had a postsynaptic effect
42
Infrequent quantal events
– likely to be driven by single vesicle release (no APs) – simplified system
43
Evidence for amplitude effect
No. of neurotransmitter in each vesicle taken to be the same
44
effects of CB1 agonists of miniature IPSCs
CB1 agonists do NOT affect: mIPSC frequency or mIPSC amplitude But DO reduce evoked IPSCs Therefore, they reduce action potential-dependant GABA release (via inhibition of Ca2+ channels)
45
2 examples of endocannabinoids
2-AG - (2-arachidonylglycerol) | Anandamide (AEA)
46
how do endocannabinoids diffuse through membranes
they are lipid soluble | not stored in vesicles
47
DSI
Depolarisation-induced Suppression of Inhibition can be mediated by CB1 receptors
48
retrograde signalling
signalling from post-synaptic cell back to pre-synaptic
49
Evidence that DSI is mediated via a retrograde messenger
1. Increase in postsynaptic [Ca2+]i is necessary and sufficient for the induction of DSI 2. The frequency of spontaneous inhibitory synaptic vesicles released from pre-synaptic is reduced 3. Postsynaptic sensitivity to exogenously applied GABA (e.g. from pipette) is not affected by depolarisation – therefore effect must be pre-synaptic 4. Not blocked by classical neurotransmitter receptor antagonists 5. DSI is not synapse or cell specific
50
effect of Ca2+ on DSI
if you block Ca2+, you block DSI
51
DSI is mediated by endocannabinoids
endocannabinoids synthesis/release is dependant on Ca2+ in response to postsynaptic depolarisation causes suppression of GABA release DSI is mimicked by blocking endocannabinoid uptake
52
psychotropic effects of cannabis mediated by which receptor
CB1
53
main effect of CB1 receptor activation
reduced inhibitory synaptic transmission
54
form of short term plasticity
DSI
55
define Ki
the concentration required to produce half maximum inhibition
56
lower Ki
means the inhibitor is more potent greater binding affinity less required to produce inhibition in 50% o
57
higher Ki
inhibitor is less potent less binding affinity more required to produce half maximum inhibition

Neuropharmacology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions