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Psychopharmacology > Hallucinogens > Flashcards

Hallucinogens Flashcards

1
Q

What is the inherent rewarding effect of hallucinogens?

A

Not inherently rewarding; may or may not produce addiction / pleasure etc

No withdrawal / physical dependence at all, generally no increases in DA

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2
Q

What are the 5 groups hallucinogens can be assigned to based on structure?

What do hallucinogens do to these synapses in each group?

A

1) Ach-like: SYNAPSES BLOCKED
2) 5-HT-like: STIMULATED synapses
3) Catecholamine-like: doesn’t say
4) Glu-like: NMDA BLOCKED
5) Opiate-like: Kappa facilitated

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3
Q

What synapses do LSD/psilocybin generally stimulate?

A

5-HT2A synapses

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4
Q

How is psychedelic experience generally elicited pharmacodynamically with hallucinogens?

A

Block cholinergic synapses
Stimulate 5-HT2A
Block NMDA synapses
Facilitate kappa-opiate synapses

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5
Q

What type of hallucinogen is scopolamine?
What receptor does it affect?

What are the phenotypic effects?

A

Anti-cholinergic; blocks muscarinic Ach

Dry mouth, blurred vision, increased heart rate, dilated pupils

(Jimson weed, belladonna)

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6
Q

What is the ED50/LD50 of jimson weed? TI?

A 
ED50 = .5mg
LD50 = 4mg

TI = 8

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7
Q

What drugs do the 5-HT agonists include?

A

Mescaline / MDMA, LSD/psilocybin

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8
Q

What receptor does belladonna / jimson weed (scopolamine) effect?

A

Muscarinic Ach receptor

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9
Q

What type of hallucinogen (pharmacodynamic) is mescaline?

A

5-HT agonist

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10
Q

What is an unpleasant phenotypic effect of mescaline?

A

Vomiting (even experienced users)

Effect in the stomach

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11
Q

What is the solubility like for mescaline?

A

Water soluble, not very lipid soluble

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12
Q

What neurotransmitter is mescaline structurally similar to?

A

NE

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13
Q

How long does it take for mescaline to reach peak CNS levels?

A

1-2hr

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14
Q

What is the state in the frontal lobes that hallucinogens cause called?

(Specifically right frontal lobe)

A

‘Hyperfrontal’ state

Hyperactive right frontal lobe; taking info in more

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15
Q

What neurotransmitter is Psilocybin similar to?

A

5-HT

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16
Q

What dose is psilocybin generally taken at? What is the half-life?

A

0.25mg/kg; effects within 30min, last 2-6hr; half-life of 3hr

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17
Q

What is the solubility of psilocybin like?

A

Quite water-soluble

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18
Q

What enzyme breaks down psilocybin?

A

MAO

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19
Q

What is the TI of psilocybin?

A

Lethal dose in humans unknown, TI quite high. Estimated 4 digits

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20
Q

What class of hallucinogens has the smallest TI?

A

Anti-cholinergics

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21
Q

What is the potency of LSD?

A

Incredibly potent; normal dose is barely visible

22
Q

What dose is generally taken for LSD?

A

25-300 micrograms (1x10^-6 g)

23
Q

How easily is LSD absorbed?

A

Readily absorbed, peak levels in 1-3hr

24
Q

Where is LSD metabolized?

A

Liver, lasts 6-8hr

25
Q

What is the TI of LSD?

A

280 (very high)

But the ED50 is super low, so you still have to be careful

26
Q

What are the effects of LSD?

A 
Slowing of time
Change in space perception
Color perception
Synesthesia
Hallucinations
27
Q

What type of receptors is the locus coeruleus full of?

A

5-HT2A

28
Q

Why will some monoaminergic neurons have action potentials on their own?

A

K+ conductance is high

Sets up K+ shunt

Shunts start to shut themselves off
Sodium leaks in as this happens

You therefore get a spike

29
Q

How often do these self-firing action potentials in monoaminergic neurons fire?

A

~1/sec (‘basal LC activity’)

30
Q

What does NE release in the LC do to glutamatergic excitation in postsynaptic neurons?

A

Enhances response of postsynaptic neurons to excitation

31
Q

Where (according to Aghajanian & Marek) do hallucinations come from?

A

Hallucinogens inhibit basal LC activity

This makes these cells more responsive to sensory inputs

So, sensory system activity is enhanced

32
Q

What is the ventral striatum involved in doing to experiences?

A

Adding motivational behavior

33
Q

According to Vollenweider and Geyer, where do hallucinogens come from?

A

Increased activity between thalamus, cortical regions, and striatum

34
Q

What drugs are the NMDA glutamate antagonists?

A

PCP

Ketamine

35
Q

What is PCP also an agonist of?

A

D-2

36
Q

How is PCP usually taken?

A

Smoked, but can be taken orally / injected. Aversive effects.

37
Q

What is the solubility of PCP?

A

Fat-soluble

LOTS of depot binding

38
Q

What is the ED50 for PCP?

A

~1mg/kg dose; LD50 at 70mg/kg

39
Q

What is the TI for PCP?

A

High double digits

40
Q

What is the LD50 for ketamine?

A

No known (safer than PCP)

41
Q

What is the solubility of ketamine?

A

Lipid & water soluble

42
Q

What effect does salvia have on 5-HT2A and NMDA receptors?

A

No effect

43
Q

What receptors does salvia effect?

A

kappa-opiate receptors, D2 receptors

44
Q

How fast are the effects of salvia when smoked? How long does it last?

A

30-60sec, lasts 10 min

45
Q

What is Ayahuasca?

A

Hallucinogenic beverage from South America

Has vines with MAO inhibitors to make it psychoactive

46
Q

How is Ayuhuasca taken into the brain?

A

Active transport across BBB

47
Q

What is the active ingredient in Ayuhuasca?

A

DMT

48
Q

How else can DMT be taken?

A

Smoked; no need for MAO inhibition

49
Q

What brain state do ketamine and PCP produce?

A

HYPO frontal (as opposed to HYPER frontal)

But they still produce hallucinations!

50
Q

What brain state exists in schizophrenics?

A

Hypofrontal

51
Q

What are two examples of 5-HT agonists?

A

Catecholamine-like drugs like mescaline or MDMA

Also serotonin-like drugs like LSD or psilocybin

Psychopharmacology (12 decks)

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