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Neuropharmacology > Cannabis - endocannabinoids and G proteins > Flashcards

Cannabis - endocannabinoids and G proteins Flashcards

1
Q

uses of cannabis

A

industrial - hemp
religious rituals
recreational use

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2
Q

recreational use of cannabis §

A

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

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3
Q

types of effects of cannabis

A

psychotropic (mainly)

somatic

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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

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5
Q

euphoria

A

heightened mood

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6
Q

episodic memory

A

recollection

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7
Q

ataxia

A

lack of voluntary control of muscle movement

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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
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9
Q

cannabis used to treat glaucoma due to

A

its ability to reduce intra-ocular pressure

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10
Q

how can cannabis be used in treatment of bronchial asthma

A

cannabis causes bronchial dilation

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11
Q

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

A

treats the nausea/vomiting caused by anti cancer drugs

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12
Q

other therapeutic uses of cannabis

A

apetite stimulant
analgesia
ataxia - to treat muscular sclerosis etc

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13
Q

mental health risks of cannabis

A 
Triggering psychotic episodes and psychosis
Increase risk of schizophrenia
Anxiety
Paranoia
Substance abuse disorders
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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)
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15
Q

legal/societal risks

A

prison sentence
fine
criminal record

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16
Q

how many cannabinoids found in recreational cannabis

A

66

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17
Q

example of cannabinoids found in cannabis

A

delta9-tetrahydrocannabinol

cannabinol

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18
Q

2 canonical cannabinoid receptors

A

CB1
CB2

known about for ages

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19
Q

other possible non-canonical cannabinoid receptors

A

GPR55
GPR119
GPR18

recently discovered

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20
Q

CB1 receptor expression

A

mainly in the brain, kidneys, liver and lungs

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21
Q

CB2 receptor expression

A

immune cells and macrophages

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22
Q

which cannabinoid receptor is a potential therapeutic target

A

CB2

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23
Q

structure of CB1 receptor

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

A

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

25
Q

which G protein subunits are CB1 receptors coupled to

A

Gi/o

26
Q

what happens when Gai/o dissociates from GB/y

A

Gai/o:

  • shuts Ca2+ channels into the cell
  • inhibits adenyl cyclase –> decreased cAMP

GB/y:
- positively regulates GIRK channels –> increased K+

27
Q

CB1 receptor location

A

ubiquitous across the brain but more densely located in higher functioning areas e.g. neocortex, hippocampus
presynaptic

28
Q

use of binding assays

A

tell us how well the radioactive ligand binds to its receptor

29
Q

assays for measuring receptor pharmacology

A

binding assays

functional assays

30
Q

use of functional assay

A

determines how activated the receptor is

measure EC50

31
Q

Ki

A

binding affinity

constant

32
Q

Ki of THC

A

10-50nM

33
Q

why does THC have a low efficacy

A

it is a partial agonist

compared to synthetic ligands

34
Q

features of synthetic ligands

A

much higher efficacy and potency

35
Q

effect of cannabidiol at CB1 receptors

A

functional antagonist

shifts the curve to the right (concentration-response curve)

36
Q

role of CB1 receptors at synapses

A

modulate inhibitory synaptic transmission

37
Q

effect of CB1 agonists

A

inhibit GABA-mediated synaptic transmission

38
Q

possible post synaptic mechanism of CB1 R agonist

A

reduce postsynaptic sensitivity to GABA

39
Q

possible pre synaptic mechanism of CB1 R agonist

A

reduce presynaptic release probability

40
Q

each quantal release

A

corresponds to each miniature IPSC

41
Q

If amplitude of events reduced …

A

then the neurotransmitter has had a postsynaptic effect

42
Q

Infrequent quantal events

A

– likely to be driven by single vesicle release (no APs) – simplified system

43
Q

Evidence for amplitude effect

A

No. of neurotransmitter in each vesicle taken to be the same

44
Q

effects of CB1 agonists of miniature IPSCs

A

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
Q

2 examples of endocannabinoids

A

2-AG - (2-arachidonylglycerol)

Anandamide (AEA)

46
Q

how do endocannabinoids diffuse through membranes

A

they are lipid soluble

not stored in vesicles

47
Q

DSI

A

Depolarisation-induced Suppression of Inhibition

can be mediated by CB1 receptors

48
Q

retrograde signalling

A

signalling from post-synaptic cell back to pre-synaptic

49
Q

Evidence that DSI is mediated via a retrograde messenger

A
  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
Q

effect of Ca2+ on DSI

A

if you block Ca2+, you block DSI

51
Q

DSI is mediated by endocannabinoids

A

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
Q

psychotropic effects of cannabis mediated by which receptor

A

CB1

53
Q

main effect of CB1 receptor activation

A

reduced inhibitory synaptic transmission

54
Q

form of short term plasticity

A

DSI

55
Q

define Ki

A

the concentration required to produce half maximum inhibition

56
Q

lower Ki

A

means the inhibitor is more potent
greater binding affinity
less required to produce inhibition in 50% o

57
Q

higher Ki

A

inhibitor is less potent
less binding affinity
more required to produce half maximum inhibition

Neuropharmacology (14 decks)

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