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Neuro-pharmacology > Endocannabinoids > Flashcards

Endocannabinoids Flashcards

1
Q

Significant THC binding was observed in the

A

cortex, basal ganglia, hippocampus, and
cerebellum

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2
Q

By 1990 researchers had cloned the gene for the
brain cannabinoid receptor (termed

A

CB1
receptor)

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3
Q

(endocannabinoids)

A

Endogenous ligands for the cannabinoid
receptors

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4
Q

Two receptors for cannabinoids are found
in humans

A

CB1
CB2

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5
Q

CB1

A

expressed widely in the CNS

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6
Q

CB2

A

is expressed primarily on immune cells

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7
Q

CB2 CNS

A

Only microglia in the CNS

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8
Q

Cannabinoid receptors are

A

G-protein
coupled receptors

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9
Q

Cannabinoid receptors are G-protein
coupled receptors

A

Mostly Gi - coupled
Rarely Gs - coupled

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10
Q

CB3

A

receptor for CBD recently proposed

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11
Q

Putative CB3
receptor for CBD recently proposed

A

GPR55 - antagonist

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12
Q

CB1receptors are

A

G-protein coupled

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13
Q

CB1
receptors are exclusively
expressed

A

presynaptically

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14
Q

CB1
receptors are G-protein coupled - primarily

A

Gi

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15
Q

CB1 Inhibitory through effects on

A

adenylate cyclase (↓ cAMP)
GIRK (↑ K+ efflux)
Ca2+-channels (↓ Ca2+ influx)

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16
Q

CB1 receptors are exclusively expressed presynaptically - Present on (3)

A

glutamatergic, GABAergic,
and monoaminergic nerve terminals

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17
Q

THC is a specific

A

partial agonist of the CB receptors.

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18
Q

Endocannabinoids are the

A

endogenous ligands for
the CB receptors

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19
Q

Endocannabinoids (2)

A

Anandamide
2-AG

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20
Q

Like phytocannabinoids (from plants),
endocannabinoids are

A

highly lipophilic

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21
Q

Endocannabinoids do not function as

A

classic
neurotransmitters

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22
Q

Endocannabinoids are capable of

A

free diffusion
through membranes

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23
Q

Endocannabinoids are capable of free diffusion
through membranes

A

They cannot be packaged into secretory vesicles

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24
Q

Primary function is

A

retrograde signaling to
modulate presynaptic neurotransmitter release

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25
Q

Release from postsynaptic compartments is
through

A

activity-dependent synthesis
mechanisms

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26
Q

Endocannabinoid
synthesis

A

Endocannabinoids are formed from
arachidonoyl-containing phospholipids

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27
Q

creation of 2-AG

A

PIP2– PLC-> DAG –DAGL-> 2-AG

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28
Q

Anandamide is similarly synthesized by

A

cleavage of phospholipids by phospholipases
A2, C, and D.

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29
Q

Post-synaptic depolarization can
activate

A

endocannabinoid synthesis

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30
Q

Endocannabinoids are released and

A

supress presynaptic GABA release

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31
Q

Endocannabinoids are released and
supress presynaptic GABA release

A

Net decrease in inhibitory transmission
leads to increased output from cell

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32
Q

Two key enzymes are responsible for
the breakdown of endocannabinoids

A

FAAH
MAGL

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33
Q

FAAH

A

metabolizes anandamide

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34
Q

MAGL

A

metabolizes 2-AG

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35
Q

A common genetic variant in FAAH (P129T)

A

decreases the rate of breakdown of anandamide

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36
Q

FAAH P129T variant is associated with a

A

a greatly reduced risk of anxiety disorder and PTSD

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37
Q

FAAH P129T mice show

A

decreased anxiety in tests such as the elevated plus maze and more rapid extinction of conditioned fear responses

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38
Q

FAAH P129T is also overrepresented in

A

problem users of street drugs, suggesting increased risk of
drug and alcohol abuse

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39
Q

Endocannabinoids are highly involved in regulation of the

A

physiological response to psychological stressors

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40
Q

Acute stress activates two distinct pathways

A

Neuronal response
Neuroendocrine response

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41
Q

Neuronal response

A

activation of the sympathetic nervous system via descending pathways from
hypothalamus

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42
Q

Neuroendocrine response

A

activation of the hypothalamic-pituitary-adrenal axis (HPA axis) leading to release of glucocorticoid hormones

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43
Q

Excess activity of the HPA axis is implicated in a number of

A

psychiatric disorders
including depression, anxiety, bipolar

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44
Q

In many systems anandamide functions as a

A

tonic (steady-state) regulator of activity
while 2-AG functions as a phasic (on demand) regulator

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45
Q

HPA Axis
regulation

A

Hypothalamic release of CRH leads to pituitary
release of ACTH into circulation, and stimulates
adrenal release of cortisol

46
Q

HPA Axis
regulation - negative feedback

A

provided by cortisol to
the hypothalamus to attenuate stress signalling
– this feedback process may be impaired in
depression and anxiety disorders.

47
Q

The limbic system provides a number of

A

modulatory inputs to the hypothalamus that are
critical in HPA response to psychological
stressors.

48
Q

Under steady-state conditions
CB1 antagonism results in

A

an
increase in glucocorticoid release

49
Q

BLA projections indirectly
provide

A

excitatory input to the
PVN

50
Q

Under conditions of stress
anandamide levels in the BLA

A

drop as
a result of FAAH induction.

51
Q

Decreased anandamide levels release
the

A

inhibitory tone leading to
excitatory output to the PVN

52
Q

CB1 agonists administered to the BLA

A

supress stress-induced activation of
the HPA axis

53
Q

Negative feedback limbic system

A

Glucocorticoids can act directly on the
hypothalamus or pituitary to provide
negative feedback preventing excess
glucocorticoid release

54
Q

Rapid feedback in the PVN can be
blocked by microinjection of

A

CB1
antagonists

55
Q

negative feedback - 2-AG levels increase resulting in

A

inhibition
of GABA interneurons

56
Q

negative feedback - Cortical output to the BNST is

A

disinhibited

57
Q

negative feedback - Net increase in inhibitory output from the

A

BNST to the PVN attenuates stress response

58
Q
  • Endocannabinoids modulate activation
    in response to
A

Stress

59
Q

AEA inhibits

A

amygdala activation

60
Q

FAAH induction

A

releases AEA
inhibitory tone on stress

61
Q

Endocannabinoids modulate recovery
from

A

stress

62
Q

2-AG synthesis in the PVN contributes to

A

rapid negative feedback

63
Q

2-AG synthesis in the PFC and HC
contribute to

A

slow negative feedback

64
Q

CB-1 is proposed to function downstream of

A

ghrelin to initiate orexigenic effects in the PVN

65
Q

GHSR signalling

A

induces
DAGL activity

66
Q

2-AG synthesis increases and signals to
presynaptic

A

CB-1 receptors

67
Q

CB-1 antagonists can block the

A

orexigenic effects
of ghrelin

68
Q
  • CB-1 agonism notably increases
A

appetite,
increases craving for highly rewarding foods, and
increases hedonic value of food

69
Q

The role of endocannabinoids in stress recovery is supported (at
least anecdotally) by

A

the intoxicating effects of cannabis

70
Q

Acute stress response - Increased blood pressure - effects of cannabis

A

Decreased blood pressure

71
Q

Acute stress response - increased sweating, water resorption
in kidneys - effects of cannabis

A

Increased thirst

72
Q

Acute stress response - Decreased gastric function,
mobilization of glucose - effects of cannabis

A

Increased hunger

73
Q

Acute stress response - Heightened awareness - anxiety - effects of cannabis

A

Anxiolysis, relaxation

74
Q

Acute stress response - Increased locomotion - effects of cannabis

A

Decreased locomotion

75
Q

Cannabidiol has a very low affinity for

A

CB receptor

76
Q
  • CBD is a weak CB1 ______ and a CB2 _____
A

CBD is a weak CB1 antagonist and a CB2
inverse
agonist but may act indirectly

77
Q

CBD paradoxically

A

potentiates the effects of THC
at the CB1 receptor by unknown mechanisms

78
Q

CBD is also a

A

a 5-HT1A receptor agonist

79
Q

CBD is also a 5-HT1A receptor agonist

A

Contribute to antidepressant and anxiolytic effects

80
Q

Cannabidiol Possible inhibitor of

A

FAAH

81
Q

CBD or high-CBD strains of cannabis have been developed for

A

therapeutic use

82
Q

High CBD cannabis is being explored as an

A

anti-convulsant for treatment resistant epilepsy
(such as Dravet syndrome)

83
Q

CBD has marked

A

antipsychotic effects in animal models of Schizophrenia

84
Q

CBD is a potent

A

antioxidant and has been shown to be neuroprotective in models of ischemic
stroke

85
Q

Rimonaban

A

synthetic CB1 antagonist – orexilytic

86
Q

Nabilone

A

synthetic THC analogue (PO) – antiemetic,
adjunct analgesic for neuropathic pain

87
Q

Dronabinol

A

(THC, PO) – antiemetic, orexigenic

88
Q

Naboximol/Sativex

A

(THC/CBD ~ 1:1) – mouth spray –
MS symptoms incl. spasticity, neuropathic pain

89
Q

CB1 Psychotherapeutics (4)

A

Rimonabant
Nabilone
Dronabinol
Sativex

90
Q

FAAH inhibitors (4)

A

Bial
Janssen
Sanofi
Vernalis

91
Q

Bial

A

killed participant

92
Q

Janssen

A

phase II trials for
anxiety/depression suspended after Bial’s adverse
events

93
Q

Sanofi

A

– failed in a trial for
depression, ongoing trials for cancer pain

94
Q

Vernalis

A

phase I trials for neuropathic
pain

95
Q

In animals, THC administration results in

A

decreased CB1
receptor expression

96
Q

Long-term, heavy users of cannabis self report

A

decreases in the subjective high

97
Q

Many suggest psychological, not physiological
dependence drives

A

addictions (e.g. behavioural
tolerance rather than pharmacodynamic tolerance)

98
Q

THC administration increases

A

VTA
firing rates and subsequent
dopamine release in the NAc

99
Q

Naltrexone

A

abolishes THC selfadministration and blocks NAc
dopamine release

100
Q

Aversive effects of THC
administration are abolished in

A

κ-opioid receptor knockout mice

101
Q

However, in human trials naltrexone
administration increased the

A

positive subjective effects of
inhaled THC administration in
regular heavy marijuana users

102
Q

Craving and difficulty stopping use are key indicators of

A

dependence in humans

103
Q

THC withdrawal can be precipitated in

A

animals

104
Q

Withdrawal symptoms to cannabis have been described
including

A
  • Irritability
  • Anxiety
  • Depressed mood
  • Sleep difficulties
  • Decreased appetite
105
Q

A major concern with the use of cannabis is the
occurrence of

A

psychosis

106
Q

Cannabis use (particularly during adolescence) is
associated with an increased risk of

A

psychosis

107
Q

Cannabis use (particularly during adolescence) is
associated with an increased risk of psychosis (2 models)

A
  • Adolescent cannabis use is causal in developing
    psychosis / precipitating psychosis in vulnerable
    individuals
  • Preclinical changes in schizophrenia are likely to predispose towards drug use
108
Q

Like cocaine and amphetamines cannabis can

A

precipitate psychosis in predisposed patients

109
Q

Alcohol, cannabis, amphetamine, or cocaine use
is often a

A

precipitant for the first psychotic
episode in schizophrenia

110
Q

Cannabis is neither necessary nor sufficient to
cause

A

psychosis or schizophrenia

111
Q
  • Cannabis use interacts with
A

genetic risk factors
for SCZ

Neuro-pharmacology (26 decks)

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