Final

Question 1

What is the core compound of LSD, DMT, and mushrooms?

Answer 1

Indoleamines

Question 2

How is MDMA different from the rest of the psychedelics?

Answer 2

It is an analgesic for DA instead of 5-HT

Question 3

What does LSD stand for?

Answer 3

lysergic acid diethylamide

Question 4

What is DMT made from?

Answer 4

the psychotria and diplopteris plant

Question 5

what is the half life of DMT?

Answer 5

15 min

Question 6

What is the MOA of MDMA? (three mechanisms)

Answer 6

• Changes 5HT monoamine transporter to an exchanger
• inhibits breakdown of 5HT via MAO and tryptophan hydroxylase
• agonist at post-synatpic 5-HT2 receptor and TAAR1

Question 7

What are the four phases of hallucinogens? What are they known for and how long do they take?

Answer 7

onset: amplification of visual stimulation (1 hr)
plateau: time slow, hallucinations intensify (2 hr)
Peak: synesthesia, euphoria/dysphoria, depersonalization, hallucinations (2-3 hr)
Offset: symptoms subside (2hr)

Question 8

Is the MOA of MDMA pre or post synaptic?

Answer 8

Most of the mechanism of pre-synaptic (a bit in the cleft)

Question 9

What parts of the brain does MDMA affect?

Answer 9

the cortex and the hippocampus of the brain

Question 10

What is the hypothesised mechanism of ego death in the brain

Answer 10

decreased activity/output of the parahippocampus

Question 11

What is an enactogen?

Answer 11

A chemical that causes increased empathy

Question 12

What does MDMA stand for?

Answer 12

Methylene dioxymethamphetamine

Question 13

What is MDMA’s structure analogous to? what does it have in addition?

Answer 13

Analogous to AMPH, but with an added oxygen ring so it can mimic serotonin

Question 14

what receptors does MDMA affect?

Answer 14

Mostly 5HT2A, but some DA, and TAAR1

Question 15

What is the MOA for MDMA?

Answer 15

Binds to pre-synaptic monoamine transporter and changes it to exchanger (uptakes MDMA and pushes out 5HT), agonist at TAAR and 5-HT2 receptors, and inhibitor of MAO and tryptophan hydroxylase

Question 16

What water-retention hormone can MDMA increase and what can it lead to?

Answer 16

MDMA increases vasopressin, which increases water in the blood stream and can lead to hyponutrina

Question 17

What is the chemical structure of mescalin?

Answer 17

tirmethoxide-phenethylamine

Question 18

What drugs are indolamines?

Answer 18

LSD, DMT, mushrooms

Question 19

what does LSD and DMT stand for?

Answer 19

lysergic acid diethylamide and dimethyl tryptamine

Question 20

What is ketonserin, risperidone, and haloperidol

Answer 20

ketonserin (5HT receptor agonist)
risperidone (D2 and 5HT receptor agonist)
haloperidol (D2 agonist)

Question 21

What are the four phases of a psychedelics

Answer 21

Onset (amplification of inputs), plateau (time slows and hallucations intensify), peak (euphora/dysphoria, ego death), and offset

Question 22

What type of drug is alcohol?

Answer 22

sedative hypnotic depressant

Question 23

What does EtOH use zero-order kinetics to get out of the blood stream versus first order kinetics?

Answer 23

There is very little ADH in the liver and so it is saturated very fast

Question 24

What is the difference between acute and long-term tolerance?

Answer 24

Acute: happens within hours and because ADH is being upregulated
long-term: happens because of metabolic shifts in the body

Question 25

What is delirium tremens

Answer 25

-A syndrome caused by acute withdrawl of EtOH after long-term use. Includes increased HR, BP, temp, along with neurological symptoms

Question 26

What is Wericke-Korsakoff syndrom

Answer 26

Brain-damage cause by LT high-dose use of EtOH. Includes fine motor problems and malnutrition

Question 27

what subunit must be present in GABA receptors in order for EtOH to have an effect?

Answer 27

Delta subunits

Question 28

what is the opioid compensation hypothesis?

Answer 28

Some people have low endogenous opioid tone, and so by upregulating the beta-endorphin cells, they can down regulate GABA and increase DA tone in the body

Question 29

What receptors are specifically correlated with EtOH long-term use?

Answer 29

NMDA receptors increased, increasing the EPSP on the cell. This potentates the Glu NMDA response and increases Ca++ levels in the cell, causing LTP

Question 30

Why doesn't curare poison the hunters that use it?

Answer 30

It is a highly charged compound, and so doesn't move into the blood

Question 31

Heroin has low affinity for its receptor, but gives better high than many other opioids. Why?

Answer 31

it is lipid-soluble and neutral charge, so it distributes quickly

Question 32

Methadone has a highly variable time of action in different ppl, why?

Answer 32

It competes with several dozen other chemicals for pGp receptors on CNS, so depending on the endogenous tone and the medications they are on, there is variable timing.

Question 33

What five key changes happen in the brains of addicted patients

Answer 33

- Molecular changes in extended reward circuit - Increased DA release from drug cue - Shift in DA dominant pathway from VTA -> NAc, to SN -> Striatum - hypofrontality in prefrontal cortex - changes in brain-stress system

Question 34

How do drugs increase cue-related DA release?

Answer 34

Cue DA is initially absent, but then start to encode reward for an activity. Drugs have really high reward DA, and so cue DA potentiates

Question 35

How do drugs change the circuitry between the midbrain and striatum and what does this lead to?

Answer 35

Drug abuse changes the primary decision pathway from the VTA to the NAc to the SN to the DLS. This changes decision from being flexible and goal oriented, so reaction and habit based.

Question 36

How do drugs change the prefrontal cortical functioning?

Answer 36

Overstimulation of the reward circuit causes repression of the striatum. This indirectly causes the repression of the frontal cortex and hypofrontality

Question 37

What is the date limiting step in alcohol metabolism?

Answer 37

AHD: alcohol dehygrenase

Question 38

What enzyme is responsible for 'asian glow'?

Answer 38

ALDH: acetaldehyde dehydrogenase

Question 39

Whats the difference between long-term and short-term tolerance of alcohol?

Answer 39

Short-term: EtOH is still high, but rxn time and cognition time is still intact Long-term: metabolic shifts leading to decreased effect of EtOH

Question 40

What is the difference between Delirium Tremens and Wernicke-Korsakoff syndrome?

Answer 40

Delirium Tremens- a neurological syndrome caused by the sudden withdrawal of EtOH or other sedatives. Wericke-Korsakoff: Brain-damage from long-term, high-dose use of EtOH. Includes tremors, nystagmus, memory disfunction, and malnutrition.

Question 41

What is the opioid compensation hypothesis?

Answer 41

People who are prone to alcohol might have an endogenous opioid tone deficiency. Alcohol inhibits Gaba interneurons, which allows to the excess excitation of DA neurons from the VTA to the NAC

Question 42

What transporters/receptors does Glu use and what do they do?

Answer 42

EAAT: Involved in Glu reuptake TAAR: intracellular endocytosis of receptors AMPA: involved in cell necrosis. It is a ligand-gated Na+ channel Kainate: involved in cell necrosis. It is a ligand-gated Na+ channel NDMA: involved in cell apoptosis. It is a ligand and voltage gated Na+ and Ca++ channel