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PSYC3030 > Cannabinoids > Flashcards

Cannabinoids Flashcards

1
Q

The major psychoactive ingredient of the marijuana plant is

a. delta6-tetrahydrocannabinol
b. cannabinol
c. anandamide
d. delta9-tetrahydrocannabinol

A

d. delta9-tetrahydrocannabinol

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2
Q

Which statement about the endocannabinoids is false?

a. They are not stored in vesicles
b. They include arachidonic derivatives such as 2-AG and anandamide
c. They are synthesized by FAAH
d. They are synthesized and released when needed, probably in response to Ca2+

A

c. They are synthesized by FAAH

NO - FAAH is an enzyme which metabolizes anandamide

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3
Q

Recent imaging studies have demonstrated some evidence of abnormalities or alterations in several brain structures, including the ___ and the ___, following chronic cannabis use.

a. hippocampus; prefrontal cortex
b. amygdala; nucleus accumbens
c. VTA; limbic system
d. hypothalamus; prefrontal cortex

A

a. hippocampus; prefrontal cortex

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4
Q

All of the following are effects that have been correlated with chronic use of marijuana except

a. adverse cardiac effects
b. development of anxiety disorders
c. damage to lung tissue
d. immune system suppression

A

b. development of anxiety disorders

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5
Q

Name the 2 endocannabinoids.

A

Arachidonoyl ethanolamide (AEA)/anandamide and 2-arachidonoylglycerol (2-AG)

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6
Q

When are endocannabinoids synthesized and released?

A

Synthesized on demand in response to Ca2+ channel opening, and diffuse out immediately

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7
Q

Why are endocannabinoids not synthesized in advance?

A

They are lipid soluble so cannot be stored in vesicles.

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8
Q

Describe non-retrograde signaling by cannabinoids.

A

Anandamide remains in postsynaptic cell and activates a cannabinoid receptor or a TRPV1 receptor

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9
Q

What is the role of TRPV1 receptors?

A

Pain, mood, motor function, learning and memory

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10
Q

Describe the relationship between endocannabinoids and glutamate.

A

Endocannabinoids activate receptors on nearby astrocytes, resulting in the release of glutamate.

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11
Q

Describe retrograde signaling by cannabinoids.

A

CB1 receptors on nearby nerve terminals are activated by 2-AG and inhibit Ca2+ mediated neurotransmitter release

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12
Q

What enzyme breaks down anandamide?

A

Fatty acid amide hydrolase (FAAH)

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13
Q

What enzyme breaks down 2-AG?

A

Monoacyl-glycerol lipase (MAGL)

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14
Q

Describe the efficacy and affinity of anandamide.

A

Low efficacy agonist (partial CB1 agonist).

High affinity

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15
Q

Describe the efficacy of 2-AG.

A

High efficacy agonist (full CB1 agonist)

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16
Q

What behaviours do endocannabinoids play a role in?

A

Regulation of fear, anxiety, stress.
Hunger, eating, and energy metabolism.
Pain regulation and neuropathic pain.

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17
Q

What is the result of CB1 antagonism?

A

Reduced food intake and hyperalgesia

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18
Q

What happens to CB1 and CB2 knockout mice?

A

Hyperalgesia

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19
Q

Describe the potency of cannabinoids.

A

Varies widely, depending on genetic strain of plant and growing conditions.

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20
Q

What is cannabis sativa?

A

Hemp; tall, woody stalks

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21
Q

What is cannabis indica?

A

Grown in India; shorter; high THC content

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22
Q

What is cannabis ruderalis?

A

Northern Europe and Asia; low THC content

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23
Q

When does cannabis use usually occur?

A

Typically begins in adolescence and peaks during young adulthood

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24
Q

What are risk factors in development of heavy marijuana use by adolescents?

A

Emotional problems, heavy drug use by family/friends, dislike of school, and early age of first use

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25
What is marijuana produced from?
Flowering hemp. | Mixture of dried and crumbled leaves, small stems, and flowering tops.
26
What is hemp?
Major source of fiber (rope, cloth, paper, oil, bird food). | Contains phytocannabinoids
27
What is the sinsemilla technique?
A way to increase THC potency by preventing pollination and seed production by female plants.
28
What is hashish? What % THC content?
Concentrated form of cannabis that can be smoked/eaten (10-20% THC)
29
What is the % THC content of marijuana?
2-5%
30
What is butane hash oil and its % THC content?
Inhaled as a vapour, up to 80% THC
31
What are three methods of consuming cannabis?
Smoking: 20-40% of THC can be absorbed. Eating: dissolve in oils contained in food; all THC enters body, but strong first pass metabolism. Dabbing: a dab is vapourized with a blowtorch or vape pen and inhaled
32
What are effective dose and latency of cannabis onset influenced by?
Amount and potency of plant, and patterns of smoking (puff volume, puff frequency, inhalation depth, breath-hold duration)
33
How much of the available THC is absorbed in the body?
5-60%
34
What does burning marijuana do to THC?
Causes THC to vapourize and enter smoker's lungs in small particles
35
How do THC levels vary after reaching peak absorption?
Plasma THC levels decline rapidly. Distributed to areas of body that have significant fatty material (brain, placenta). Half-life of 20-30 hours, and metabolites are found up to 2 weeks later. By 2 hours, levels have dropped significantly
36
At what THC plasma level is a "high" experienced?
5-10 ng/mL
37
What is cannabidiol?
Similar in structure to THC, but a lower affinity for cannabinoid receptors. May have therapeutic potential because it lacks intoxicating and dependence-producing effects of THC
38
Where are CB1 receptors found? What type of receptors are they?
CNS. | Metabotropic receptors that inhibit cAMP formation, inhibit V-gated Ca2+ channels, and open K+ channels.
39
Where are CB2 receptors found? What type of receptors are they?
Immune system and other tissues such as bone, adipose cells, and GI tract. Metabotropic receptors that inhibit cAMP formation, inhibit V-gated Ca2+ channels, and open K+ channels
40
What is the mechanism of action of CB1 receptors?
They are found on axon terminals. They inhibit release of many neurotransmitters. They also modulate gene expression by activation of MAP kinase. They also cause epigenetic changes such as DNA methylation, contributing to long-term consequences
41
How do cannabinoids affect LTP?
Cannabinoids inhibit the induction of LTP in hippocampal CA1 area
42
What are the four stages of behavioural effects from cannabis?
The "buzz" - lightheadedness, dizziness, tingling. The "high" - euphoria, exhilarations, disinhibition, laughter. "Stoned" - calm, relaxed, dreamlike state. "Comedown" - gradual cessation of effects.
43
What are some side effects of cannabis use?
``` Transient psychotic symptoms (depersonalization, derealization, agitation, paranoia). Memory impairment (verbal, visual, visuospatial episodic, semantic, working), deficits in verbal learning, attention, inhibitory control, and psychomotor function. Affects psychomotor performance (deficits in driving ability due to reaction time, divided attention, critical tracking deficits) ```
44
What are the effects of chronic cannabis use in young people?
Deficits in educational performance, cognitive deficits (aimlessness, decreased motivation, lack of planning, decreased productivity)
45
What behaviours do mice given THC exhibit?
Reduced locomotor activity, hypothermia, catalepsy, and hypoalgesia
46
How does pretreatment with rimonabant affect THC consumption?
Lever pressing for THC was blocked by pretreatment with rimonabant, indicating that reinforcing effect was dependent on CB1 activation
47
Is there an interaction between endocannabinoid and endogenous opioid systems? If so, in what respect?
Yes. Reinforcement, dependence, relapse for ethanol, nicotine, cocaine.
48
How does tolerance to CB1 agonists occur?
Combination of desensitization and down-regulation of CB1 receptors; aligns with PET imaging studies
49
What is the result of cannabinoid repeated exposure in adolescent rodents?
Changes in glutamatergic, GABAergic, and DA systems. Altered synaptic plasticity, dysregulated emotional/social behaviours, impaired cognitive function. Deficits in prefrontal pyramidal cell dendritic development
50
How does reinforcement due to cannabis consumption occur?
Cannabinoids stimulate firing of DA neurons in VTA and enhance DA release in NAcc. Indirect effect as CB1 receptors are not expressed by DA neurons. Cannabinoids activate CB1 receptors in GABAergic interneurons of VTA, reducing local GABA release
51
What are some physiological effects of cannabis consumption?
Increased blood flow to skin, flushing, increased HR, increased hunger
52
How does chronic cannabis use affect the brain?
Lower volume in hippocampus and prefrontal cortex, white matter deficits, and substantially impaired DA function in striatum
53
What other systems are affected by cannabis use?
Respiratory system (can damage lungs), cardiovascular system, reproductive system, immune system (suppresses immune function by CB1 and CB2 receptors and impairs resistance to bacterial/viral infections)
54
How does maternal cannabis use during pregnancy affect the fetus?
Decreased body weight and head circumference, startles and tremors, decreased habituation to light, and altered sleep EEG
55
How many users become dependent?
10-25% of users become dependent, and 50% of those who progress to daily use
56
What can be seen in those who have strongest withdrawal symptoms from cannabis on the molecular level?
Lowest levels of receptor binding
57
What are withdrawal symptoms from cannabis?
Irritability, increased anxiety, depressed mood, sleep disturbances, aggressiveness, decreased appetite
58
What does cannabis dependency treatment involve?
CBT, relapse prevention training, motivational enhancement therapy, contingency management, vulnerable to relapse
59
What is cannabis use disorder?
Temporary condition that usually resolves over time. | Average duration of 32 months.
60
What are the factors contributing to the development of cannabis use disorder?
Genetic factors, early onset, positive reactions, coping with negative emotions, life stressors, living alone, concurrent use of other drugs, and being male

PSYC3030 (12 decks)

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