Stimulants and Psychomimetics

Question 1

Amphetamines have the net affect of G in the Q and F areas of the brain.

Answer 1

Increase of dopamine transmission in the MESOLIMBIC and MESOCORTICAL areas.

Question 2

Amphetamine increases cytoplasmic (transporter mediates) or vesicular (vesicle-mediated) release?

Answer 2

Cytoplasmic.

Question 3

In what six ways does amphetamine increase dopamine signalling?
Two to do with NAd, confusingly. One to do with degradation, one is really non-specific, another to do with transport and leaves it one tad different.

Answer 3

Blocks reuptake/reverses DAT1 transporter
Induces release from vesicles into cytoplasm
Inhibits MAO degradation
Increases DA release.

Block NAd reuptake
Increase NAd release.

Question 4

The points about amphetamine PK.

Answer 4

Readily absorbed inc. BBB
PkA = 9 (poorer excretion the higher the pH)
Excreted through urine (test your pee)

Question 5

What’s one thing about amphetamine that can make it more addictive than cocaine?

Answer 5

Duration of action and withdrawal effects last an order of magnitude longer than cocaine.

Question 6

What is the basis of psychological/personality disturbances that come with chronic use of amphetamines?

Answer 6

Cell death, due to accumulation of reactive metabolised.

Question 7

What are 4 signs of toxic psychosis from prolonged amphetamine use?

Answer 7

vivid hallucinations
paranoid delusions/compulsions
marked weight loss

Question 8

Insomnia, extreme lethargy, depression, anxiety, hyperphagia, are experienced in what situation?

Answer 8

Amphetamine withdrawal.

Question 9

Two effects of amphetamine show rapid tolerance.

Answer 9

Euphoria and anorexia

Question 10

What’s the difference between crack and normal cocaine?

Answer 10

Cocaine hydrochloride is the powder version. Crack has undergone further processing by dissolving the HCl, alkalinising it and extracting the base with an ether.

Question 11

T or F: Tolerance develops rapidly with cocaine and people have to take more to get the same effect.

Answer 11

FALSE. Tolerance is there but not really experienced by users. The dependence is more psychological. (Separate from the addiction).

Question 12

What is the active ingredient of weed?

Answer 12

∆9 tetrahydrocannabinol (THC).

Question 13

CBX mediates the peripheral effects of weed. CBY mediates the psychotropic ones.

Answer 13

CB1: brain and mind
CB2: peripheral

Question 14

What are two medical applications you’ll hear are promising for weed?

Answer 14

Glaucoma
During chemotherapy (antiemesis)

Question 15

Apart from the CB1&2 GCPR partial agonism, what else is a mechanism of THC?

Answer 15

D1>D2

D1 activation and D2 inhibition

Question 16

Why would you never use urinary alkalisation as a response to amphetamine overdose?

Answer 16

Because it’s Pka is 9.0. That means it’s excretion is better at low pHs and a urinary pH higher than 7 would be crap for amphetamine excretion.

Question 17

How long does cannabis withdrawal last (mild)

Answer 17

4-5 days.

Question 18

How does the mechanism of synthetic cannabinoids differ from the real thing?

Answer 18

FULL agonists of CB1&2.

Question 19

Synthetic cannabinoids have a much higher affinity for X than Y.

Answer 19

CB1 than CB2.

Question 20

Why are synthetic cannabinoids crap?

In what respect is it flat out anti-marijuana?

Answer 20

The peripheral effects and withdrawal symptoms are just fucking awful.
It’s anti marijuana in that it causes nausea and wretching.
CV overdrive.
Withdrawal include extreme anxiety/depression (suicides) and coronary ischaemia.