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Behavioral Pharmacology > Chapter 14: Marijuana and Cannabinoids > Flashcards

Chapter 14: Marijuana and Cannabinoids Flashcards

1
Q

amotivational syndrome

A

Symptoms of cannabis use that relate to poor educational achievement and motivation.

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2
Q

anandamide

A

arachidonoyl ethanolamide; Common chemical name of the arachidonic acid derivative that functions as an endogenous ligand for cannabinoid receptors in the brain.

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3
Q

2-arachidonoylglycerol (2-AG)

A

An arachidonic acid derivative that functions as an endogenous ligand for brain cannabinoid receptors

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4
Q

cannabinoid receptor

A

Receptor for cannabinoids, including THC and anandamide. In the CNS, they are concentrated in the basal ganglia, cerebellum, hippocampus, and cerebral cortex.

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5
Q

cannabinoids

A

Collection of over 60 compounds found uniquely in cannabis plants.

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6
Q

CB1

A

Cannabinoid receptor of the metabotropic receptor family located in the CNS; play a role in the reward system

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7
Q

CB2

A

Cannabinoid receptor located primarily in the immune system, but also in bone, fat cells, and the GI tract. Are also expressed by microglia

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8
Q

Δ9-tetrahydrocannabinol (THC)

A

Psychoactive chemical found in cannabis plants; a cannabinoid.

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9
Q

endocannabinoids

A

Lipid-like substances that activate CB receptors. They are produced from arachidonic acid in the body.

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10
Q

fatty acid amide hydrolase (FAAH)

A

Enzyme that metabolizes endocannabinoids

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11
Q

hash oil

A

Potent oil that is derived from hashish and contains a high concentration of cannabinoids

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12
Q

hashish

A

Type of cannabis derivative that is smoked or eaten.

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13
Q

hyperalgesia

A

Condition characterized by an increased sensitivity to pain.

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14
Q

monoacylglycerol lipase (MAGL)

A

Enzyme primarily responsible for metabolism of the endocannabinoid 2-arachidonoylglycerol.

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15
Q

precipitated withdrawal

A

Method used to test dependence and withdrawal by administering an antagonist to block drug effects rapidly.

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16
Q

retrograde messenger

A

Chemical synthesized and released by a postsynaptic cell that diffuses into the nerve terminal of the presynaptic cell, often for the purpose of altering neurotransmitter release by the terminal.

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17
Q

rimonabant

A

SR 141716; Antagonist selective for the CB1 receptor. It is also called SR 141716.

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18
Q

sinsemilla

A

The potent marijuana produced by preventing pollination and seed production in the female cannabis plants.

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19
Q

how much THC is in a joint?

A

a joint is .5-1 gram of cannabis and 1 gram of cannabis contains 40mg or THC, but only 20-30% is absorbed into the lungs

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20
Q

smoking THC

A

readily absorbed through the lungs resulting in rising levels in the blood plasma

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21
Q

oral consumption of THC

A

leads to prolonged but poor absorption resulting in low and variable plasma concentrations—because of degradation in the stomach and first pass metabolism

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22
Q

what is THC converted into?

A

metabolites– 11-hydroxy-THC and 11-nor-carboxy-THC which are excreted mostly in the feces

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23
Q

half life of THC

A

20-30 hours

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24
Q

what family of receptors do cannabinoid receptors belong to?

A

metabotropic receptors

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25
Q

how do metabotropic receptors (and thus cannabinoids) exert their effects?

A

coupling with G proteins Gi and Go which inhibits cyclic adenosine monophosphate (cAMP) formation, inhibits voltage sensitive Ca2+ channels, and activation of K+ channel opening

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26
Q

where do CB1 receptors exist?

A

axon terminals

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27
Q

what happens when CB1 receptors are activated?

A

by activating these presynaptic receptors, cannabinoids can inhibit the release of many different neurotransmitters including acetylcholine, dopamine, norepinephrine, serotonin, glutamate, and GABA

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28
Q

is THC a full CB1 and CB2 agonist?

A

nope–it is a partial agonist

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29
Q

what are the synthetic cannabinoid agonists?

A

CP-55,940 and WIN 55,212-2

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30
Q

what does administration of THC to mice lead to?

A
  1. reduced locomotor activity
  2. hypothermia (decrease in core body temp)
  3. catalepsy (muscular rigidity)
  4. hypoalgesia (reduced pain sensitivity)
    - -all mediated by CB1 receptors
31
Q

cannabinoids and learning

A

they disrupt memory in several different kinds of learning tasks; it inhibits the induction of long-term potentiation (LTP) in the hippocampal CA1 area; CB1 activation in the hippocampus underlies spatial learning deficits

32
Q

what effects to CB2 agonists exert?

A

inhibit the release of cytokines (immune cell signaling molecules such as interleukins and interferons) and can stimulate or inhibit the migration of immune cells toward the site of an inflammatory reaction

33
Q

what is the principle endocannabinoid for both CB1 and CB2 receptors?

A

2-AG

34
Q

endocannabinoid release

A

they are made and released when needed; the rise in intracellular Ca2+ levels trigger release

35
Q

what happens after endocannabinoids are released?

A

they are removed from the extracellular fluid by uptake mechanisms

36
Q

potential endocannabinoid uptake mechanisms

A
  1. uptake by means of a protein carrier in the cell membrane
  2. uptake by simple passive diffusion across the cell membrane
  3. uptake by means of anandamide binding to a membrane protein followed by endocytosis of the anandamide-protein complex
37
Q

how are endocannabinoids metabolized?

A

by several enzymes

  • anandamide is broken down by fatty acide amide hydrolase (FAAH)
  • 2-AG is broken down by monoacyl-glycerol lipase (MAGL)
38
Q

are endocannabinoids retrograde messengers?

A

yes–at specific synapses in the hippocampus and cerebellum

39
Q

how do endocannabinoids work as retrograde messengers?

A

they are synthesized and released in response to depolarization of the postsynaptic cell due to the influx of Ca2+ through voltage-gated Ca2+ channels. they then cross the synaptic cleft, activate CB1 receptors on the nerve terminal and inhibit ca2+ mediate neurotransmitter release from the terminal

40
Q

endocannabinoids as second messengers in the hippocampus

A

they are generated by pyramidal neurons and diffuse to nearby terminals of GABAergic interneurons that normally suppress the firing of the pyramidal cells. The resulting inhibition of GABA release temporarily permits the pyramidal cells to fire more rapidly

41
Q

endocannabinoids and pain

A

they act on both CB1 and CB2 to modulate pain perception

42
Q

endocannabinoids and hunger

A

CB1 receptor antagonists reliably reduce food consumption; they enhance incentive motivational properties of food and food mediate reward; possible treatment for obesity

43
Q

endocannabinoids and fear

A

play a great role in the extinction of learned (fear) responses; CB1 knockout mice do not show normal extinction; endocannabinoids released during extinction and acting on CB1 receptors in the basolateral amygdala alter synaptic plasticity in a manner that enables the animals to learn that the tone is no longer dangerous; involved in the alleviation of fear; increased anandamide levels due to reduced FAAH activity enhance the ability to turn off neural and behavioral responses to threatening stimuli

44
Q

stages of marijuana use

A
  1. buzz- brief period of initial responding during which the user may feel lightheaded or even dizzy; tingling sensations
  2. high- feelings of euphoria and exhilaration; sense of disinhibition
  3. stoned- user usually feels calm, relaxed, perhaps even in a dreamlike state; floating sensations, enhanced visual and auditory perception, visual illusions, and a tremendous slowing of time passage
  4. come down- gradual cessation of effects
45
Q

physiological responses

A

increased blood flow to the skin, warmth and flushing, increases hunger, stimulated heart rate

46
Q

what determines high?

A

it is dose dependent and partially mediated by CB1 receptors

47
Q

negative side effects

A

psychotic symptoms, depersonalization, derealization, agitation, paranoia

48
Q

when does the maximum level of intoxication occur?

A

when plasma THC concentrations are already declining

49
Q

cognitive deficits

A

illogical or disordered thinking, fragmented speech, difficulty in remaining focused on a given topic of conversation; heavy usage may eliminate cognitive effects

50
Q

memory

A

cannabinoids appear to interfere with all aspects of memory processing–encoding, consolidation, and retrieval; can be reversed in 2-3 weeks after stopping

51
Q

what can heavy use impair?

A

executive functioning

52
Q

psychomotor functioning

A

can impair it especially under demanding task conditions (driving)

53
Q

reward/reinforcement

A

one factor in cannabinoid reinforcement may be activation of the mesolimbic dopamine (DA) system as cannabinoids stimulate firing of DA neurons in the VTA, and to enhance DA release in the nucleus accumbens; close interactions between cannabinoid and opioid systems (opioid agonists enhance cannabinoid self-administration)

54
Q

factors that influence early marijuana use

A

lax parental monitoring and early behavioral problems, early conduct problems

55
Q

risk factors for heavy early marijuana

A

emotional problems in family, heavy drug use in household or by peers, dislike of school, poor school performance, early age of first use of marijuana

56
Q

early positive experiences with marijuana

A

lead to greater risk of later dependence

57
Q

tolerance

A

repeated exposure to THC and other CB1 agonists developed profound tolerance to the behavioral and physiological effects; mostly parmacodynamic involving both desensitization and down regulation of CB1 receptors

58
Q

dependence

A

10% of users will become dependent; difficulty in stopping one’s use, craving, unpleasant withdrawal

59
Q

withdrawal symptoms

A

irritability, increased anxiety, depressed mood, sleep disturbances, heightened aggressiveness, and decreased appetite; symptoms are greatest during first 1-2 weeks

60
Q

abstinence syndrome

A

decreased DA cell firing in the VTA and reduced DA release in the nucleus accumbens, increased corticotropin-releasing factor (CRF) release in the central nucleus of the amygdala, increase secretion of stress hormones, and changes in the endocannabinoid system

61
Q

educational performance

A

greater use is associated with poorer grades, more negative attitudes about school, and increased absenteeism

62
Q

IQ

A

the amount of cannabis use and the appearance of symptoms of cannabis dependence were significantly associated with neuropsychological impairment, including lower IQ at age 38 even after controlling for educational attainment

63
Q

psychiatric features

A

significant relationship between early heavy marijuana smoking and increased risk for the later development of psychotic disorders such as schizophrenia

64
Q

carcinogens

A

tar from cannabis smoke actually contains higher concentration of certain carcinogens known as benzanthracenes and benzpyrens; the amount of car and carbon monoxide taken in per cigarette are much greater for marijuana joints than for tobacco

65
Q

respiratory symptoms

A

chronic cough, increased phlegm, wheezing, bronchitis

66
Q

immune function

A

CB1 and CB2 receptors are expressed by various immune cells and activation of these receptors generally suppresses immune function; THC has been found to impair an organism’s resistence to bacterial and viral infections

67
Q

reproductive system

A

THC suppresses the release of luteinizing hormone (LH), an important reproductive hormone secreted by the pituitary gland in males and females.

68
Q

animals and pregnancy

A

pregnancy failure, retarded embryonic development, fetal death

69
Q

male reproduction

A

reduce testosterone levels, sperm counts, and sperm motility

70
Q

association model

A

individuals who are already vulnerable to developing psychosis have an increased likelihood of using cannabis when they’re young

71
Q

causal model

A

cannabis use predisposes individuals to develop psychosis later in life

72
Q

indicator-variable model

A

one or more other factors lead jointly to cannabis use and psychosis proneness

73
Q

prenatal marijuana exposure

A

cognitive deficits, poor school achievement, increased risk for tobacco/ marijuana use later in life have all been associated with prenatal marijuana exposure

Behavioral Pharmacology (11 decks)

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