Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

C PSYC 462 > WEED > Flashcards

WEED Flashcards

1
Q

What is marijuana made from?

A

flowering hemp (cannabis sativa)

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

what was hemp used for?

A

fiber was used for rope, cloth, paper

medical reasons too!

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

what are active ingredients in marijuana classified as?

A

hallucinogens

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

what are the main compounds in marijiana

A

there are 70 unique compounds: cannabinoids, plus 400 identified ones
main ones:
psychoactive: THC
CBD: lower affinity for receptor, lacks intoxicating effects but maybe medicinal effects?

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

what does marijuana act as an agonist on?

A

endogenous neurochemical system: endocannabinoids

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

where is cannabinoid receptors expressed?

A

hippocampus, stritum, nac, pfc and amygdala

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

what are the 2 types of receptors?

A

CB1: CNS (main effects)
- heteroreceptors to inhibit release of NTs
CB2: immune system, bone, fat cells, GI tract

Metabotropic (inhibitory)

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

what are the effects of THC on CB1 receptors?

A

reduced locomotion, hypothermia, hypoalgesia, hyperphagia, cognitive deficits (CB1 recpetors)

if you block CB1 receptors with antagonist (rimonabant) you see reduction in these effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is rimonabant?

A

CB1 receptor antagonist

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

What are the two main endocannabinoids?

A

Anadamine (AEA): partial agonist -weight loss drug that caused depression
2-AG: full agonist
- on CB1

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

describe metabolism of endocannabinoids?

A

anadamine: FAAH (fatty acid amide hydrolase)
2-AG: MAGL (monoacyl glycerol lipase)
- if you block these enzymes you increase endocannabinoid transmission

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

Describe retrograde transmission.

A
  • endocannabinoid synthesized on demand in response to depolarization and increased calcium influx on post syanptic cell.
  • cross cleft (cause its lipid soluble) and activate CB1 receptors on nerve terminals (often GABA or glutamate terminals)
  • net effect varies on cell type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe 2 other ways cannabinoids effect neural activity

A

non retrograde: anadamine activated a cannabinoid or TRPV1 (ion channel that causes depolarization) on postsynaptic cell

Activate receptors on nearby astrocytes resulting in extrasynatpic glutamate relase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is TRPV1 responsible for?

A

depolarizing ion channel.

processing pain, mood, motor function, learning and memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the functions of endogenous cannabinoids?

A
  • clarified through antagonist and KO mice
    Pain perception
    Nausea
  • used as a cancer treatment for these 2 reasons
    Feeding/appetite
    learning/memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe pain perception of cannabinoids? what type of pain is it most effective at treating?

A
  • reducing CB1 transmission increases pain sensitivity
  • stimulating cb1 receptors with agnoinsts reducies pain sensitivity
  • work in brain and spinal cord
  • effective at treating neuropathic pain (in cns not body) while opiods suck at this.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe nausea function onf canabioids

A

increasing cannabinoid activity reduces nausea and vomiting for a variety of conditions
- site of action in medulla (CNS)and gut (PNS)

18
Q

describe feeding behaviors of cannabinoids?

A

enhance motivational properties of food and stimulate appetite.
- CB1 receptors reduce food consumption in animals and humans
- Brain and GUt effects
AM6545 CB1 antagonist acts on periphery (doesn’t cross BBB) and reduces fod intake

19
Q

describe the learning and memory effects of endocannabinoids?

A

extinction of learned responses rather than acquisition.
- they don’t lose their fear conditioining (can’t overwrite the memory)

CB1 KO mice do not show normal extinction of freezing response (same with antagonists)
- maybe they have a role in overwriting previously established memories (or emotional associations)

20
Q

How is marijuana absorbed and metabolized? describe blood levels

A

inhaled or orally (oral is lower and more variable)
Vaporized: easy to absorb THC particles that enter lungs, rapid rise in blood levels

  • dose, potency of plant, patterns of smoking (breathold) have an effect

concentrations decline because of liver metabolism and accumulation in fat stores (its very lipid soluble)
- rapid decline not just liver but cause its dispersing in the body and brain.

complete elimination is much slower cause its stored in fat tissues
- slowly leaks out ( weeks or months)

21
Q

what is marijuana’s half life?

A

+ 20 hours

22
Q

what is reverse tolerance?

A
  • reverse tolerance (not feeling high the first time) may be related to becoming more experienced and holding breath better.
23
Q

what are the subjective effects of marijuana?

A

buzz, high, stoned, come down.

24
Q

what are physical responses to marijuana?

A

heart rate, bloow flow, eyes flushing increased hunger

transient psychotic symptoms (depersonalization, derealization, agitation, paranoia (its adverse for some people)

Placebo can produce these effects too

25
Q

when does maximum intoxification occur?

A

when plasma levels of THC are declining, after cigarette is finished.
not yet equilibrated when plasma peaks, due to diffusions of THC between brain, plasma and fat stores.

26
Q

how does weed effect your behavior?

A

cognitive and psychomotor performance
- impairs spatial verbal memory, time estimation, reaction time, intefere with all aspects of memory (encoding, consolidation, retrieval)

  • similarly induced in animals (systemically or in hippocampus)
27
Q

effects of weed with chronic use?

A

no overdose reports
smoking can damage lungs
reduce testosterone in men
impair immune resistance and adverse effects on fetuses (animal studies)

Impaired executive functioning for 2-3 weeks after stopping use. (some long term users show even more impairment PFC kinda stuff )

28
Q

how does chronic weed use effect youth

A

In youth: inversely related to academic performance, linked to amotivational syndrome (but we don’t know if that’s a preexisting trait or not)

29
Q

what brain abnormalilites is chronic weed use related to?

A
  • Anterior cingulate (frontal lobes) regulating emotional and behavioral inhibition.
  • chronic users showed reduced activation here (in response to faces) meaning that they have maybe a deficit in appropriately judge emotional cues.
30
Q

What is weed’s link to schizophrenia?

A

Smoking in youth with genetic predisposition can lead to schizophrenia (val/val + smoking = schizo)
- Polymorphism in COMT (metabolizes dopamine faster in frontal lobes)

31
Q

What is weed’s link to dopamine?

A

chronic cannabis is linked to impaired dopaminergic function in striatum, may play a role in long term mood disturbances, motivation, cognition, cannabis use disorders

32
Q

Are cannabinoids reinforcing?

A

Driven by CB1 receptors

  • regular users can tell THC from placebo and prefer it.
  • blocking CB1 receptors reduces effects

Animals: story unclear. One monkey study did self administer, blocked by CB1 antagonist rimonabant.

Rodents don’t self administer THC tho
- they have administered CB1 agonists, and show a place preference but only when exposed in home cage. other studies can’t replicate this.

THC less reinforcing compared to other drugs in animals.

Implicated in reinforcement, dependence and relapse for ethano, nicotine and cocaine.

33
Q

How does weed effect PFC and striatum DA levels?

A

THC: increases PFC DA
THC: mixed results for striatal DA (even tho other cannabinoid drugs increase DA in accumbens)
- cannabinoids stimulate firing of DA neurons via inhibiting GABA release in VTA (cause there are no CB1 receptors on DA neurons)

  • in other drugs, they all activate mesolimbic DA pathway
34
Q

How do opiods work with cannabinoids?

A

reinforcing effects mediated by opiods possibly (in the monkey study, if opioid antagonist was give, it reduced self administration
-unclear in humans

35
Q

Describe tolerance to marijuana.

A

repeated exposure causes tolerance.

- pharmodynamic tolerance (desensitization and down regulation)

36
Q

Describe withdrawal to marijuana

A

high doses of THC leads to withdrawal in animals udner certain conditions (tremors, shakes, increased grooming, hunched)
- easier with precipitated withdrawal (not really spontaneously occuring)

in humans: after chronic use is much less severe (102 weeks): irritability, increased anxiety and aggressiveness, depressed mood, sleep disturbances, decreased appetite

  • maybe its not so bad because it stays in body for so long?
37
Q

what is precipitated withdrawal?

A

give animal large amounts of drug,then give then an antagonist and see withdrawal symptoms

38
Q

what is dependence to marijuana?

A

manifested as a difficulty stopping use, craving for marijuana, unpleasant withdrwawl symptoms.
- risk of dependence is related to USE patterns.
people who use it daily have 50% probability of becoming dependent.
- driven by withdrawal symptoms usually

39
Q

Describe the switch from recreational to chronic use?

A

5% people used it in some way. begins in adolescence and peaks in young adulthood

  • not tried it by mid twenties, less likely they will start it
  • don’t show addictive profile of other drugs (alcohol, nicotine, cocaine)

10% of those who use it become dependent

  • overall risk is 20-25%
  • usually temporary and recovery rates are higher
40
Q

is weed a gateway drug?

A

no. risk factors that lead to heavy maijiana use are the same for hard drug use (family problems, drug use by family/peers, dislike school, early age)

users with early postive responses to use have greater risk of becoming dependent

harder drug use decreased after legalization

but its best not to use in adolescence cause brain is developing and weed has effect in the brain.

C PSYC 462 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions