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Neuropharma Of CNS disorders > Psychoactive Drugs > Flashcards

Psychoactive Drugs Flashcards

1
Q

Psychotometric, psychotropic and psychoactive

A

Drugs that alter perception, behaviour and mood

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2
Q

Hallucigens

A

Alter perceptions, thoughts and feelings eg LSD and psilocybin

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3
Q

Caapi

A

Naturally occurring hallucinogen
Active constituent - harmakine
Motor control but altered perception

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4
Q

Peyote

A

Active constituent - mescaline

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5
Q

Hallucinogen potency

A

Psilocybin - 250 ug for 3 hrs
Mescaline 15 mg for 12
(Psilocybin more potent)

LSD 3ug for 10 hrs (first synthetic drug)

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6
Q

LSD history

A

Clinical use against st anthonies fore (Vado construction of peripheral blood vessels and psychosis) Caused by Ergot alkaloids - but used as hemorages treatment

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7
Q

LSD

A

Derivative of naturally occurring ergots
Caused peripheral vasoconstriction
Effects: somatic (motor and autonomic), perceptual (hallucinations), psychological (synaesthesia)

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8
Q

Cross tolerance (LSD)

A

Tolerance acquired from use of one for both
Mescaline and LSD
Both act at same class receptor site
Both similar to 5-HT

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9
Q

How does LSD act in the periphery

A

As a 5ht2 receptor antagonist

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10
Q

How does LSD work in the brain

A

As a 5ht receptor agonist/partial agonist
5HT synapses release, postsynaptic receptors acted on
Presynaptic auto receptors, 5HT acts on this to fine tune release of 5HT on synapse, -ve feedback loop, 5 HT in synaptic cleft activate these which inhibit release of 5HT

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11
Q

LSD administered, 5HT antagonist. Does metabolite increase or decrease

A

Increase

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12
Q

LSD agonist. Increase or decrease metabolites?

A

Decrease

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13
Q

Where does LSD have its affect in the brain?

A

Potentially Reticular activating formation

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14
Q

Reticular formation

A

Sensory afferents arise and project to brain, synapse in thalamus, thalamus neurones project to primary somatosensory cortex (direct, modality specific) - raphe nucleus, locus coerelous

Axon collaterals, synapse within reticular formation, neurones project to thalamus or broad cortex (indirect, non specific arousal)

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15
Q

LSD impact on raphe neurones

A

LSD decreases firing rate of raphe neurones (5HT1A receptor)
(Raphe neurones send extensive projection to the forebrain)
Dendritic nucleis in raphe nucleus, release 5HT from dendrutes, act on Austin receptors, inhibit activity
LSD acts as 5HT1a partial agonist, decreasing firing rate of neurones

Other drugs don’t do this so not cause of hallucinations

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16
Q

What affect does lesioning the raphe nucleus cause

A

Can still discriminate between saline and LSD
So not key in main experiences of alterations in perception

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17
Q

LSD impact on noradrenergic pathway

A

LSD increases activity in locus coeruleos neurones
LSD increases activity of subsets of neurones in cortex
(Increase release of noradrenaline)

Direct and indirect (noradrenaline and 5HT2 receptors)

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18
Q

Where are 5HT2A receptors found

A

Temporal and prefrontal cortex, and thalamus (processes somatosensory inputs and recieved afferents from locus coeruleus)

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19
Q

Does LSD exerts it’s effects through 5HT2A receptors?

A

Both LSD and phenethylamines use same receptor
Correlations - highest affinity = most potent, least affinity = less potent

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20
Q

LSD perception theory

A

Acts on 5HT2A receptors, highly expressed in cortex, pyramidal neurones, increases activity of layer 5 pyramidal neurones
Imaging studies

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21
Q

Entropic effect

A

Massive activation of different neuronal regions during visual stimulus

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22
Q

Psychotomimetic drugs

A

Phencyclidine (PCP)
Dissociative anaesthetic (same class as ketamine)
Catatonic state
Caused emergence phenomenon (psychotic symptoms, altered body image, cognitive disorganisation, hypnagogic states, euphoria, apathy, hallucinations

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23
Q

PCP interacts with what receptors

A

Sigma opiate receptor - modulates NAdr release (presynaptic terminals)

Antagonist of NMDA (glutamate receptor), ligand gated ion chancel, excitatory, non selective ion - PCP blocks channel, increased conc of PCP = increased firing rate subcorticotical doperminergic excitation

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24
Q

NMDA

A

Expressed in GABA Neurones in subcortical regions of the brain. Regulated by projections from the cortex

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25
Action of PCP
Cortical neurones project to NMDA receptors releasing glutamate, activates inhibitory neurones so inhibits dopermenergic neurones I’m VTA PCP blocks NMDA receptors and so dopermenergic neurones remain activated causing increased activity of subcortical region
26
Hallucinogenic drugs as models for schizophrenia
LSD and PCP used in animal models for schizophrenia
27
Drugs acting on catecholamine neurotransmission
Cocaine and alcohol Associated with deaths
28
Cocaine
Peesynaptic neurones release catacholamine neurotransmitters High affinity uptake transporter (transports back into nerve terminal Cocaine Blocks high affinity reputable So increase catacholamine in synaptic cleft Enhance catercholoergic transmission
29
Actions of cocaine
Local anaesthetic (blocks voltage gated NA channels) Euphoria Appetite suppressant Big dose- tremors, convulsions, CNS depression Susceptible individuals - toxic psychosis (similar to schizophrenia) Addictive properties
30
Amphetamine
Sympathomimetic amine - mimics effects of sympathetic nerve stimulation
31
Actions of amphetimine
Appetite suppressant Causes euphoria Hypertensive Used: weight control, narcolepsy, ADD Can cause psychosis
32
How does amphetamine work?
Reverse transport Binds to transporter on extracelluar face and reverses transport so dopamine out and AMPH in Elevates catacholamine transmitters
33
MDMA
Effects on empathy, sense of well being Similar pharma to cocaine and amphetamine
34
How does MDMA work?
Increase 5HT by decreasing 5HT serotonin uptake. Blocks MAO (responsible for metabolism of NTs) Repeated use = toxic. Degeneration of raphe neurones
35
Addiction
Persistent disorder of brain function in which compulsive drug use occurs despite serious negative consequences for affected individual. Physical and psychological dependence
36
Physical dependence
Withdrawal symptoms eg shaking, diohrea Usually opposite of drug effects
37
Psychological dependence
Craving Brain adapts to presence of drug. Feedback- homeostatic maladapted/adapted
38
Features of addiction
Compulsion to take drug Positive and negative reinforcement 1. Withdrawal syndrome 2. Tolerance
39
Which brain region contains dopaminergic neurones?
Ventral techmental area
40
Psychotomimetic drugs with abuse potential have common actions on the limbic system of the brain
Key focus in addiction: Ventral tegmental area which projects to nucleus accumbens
41
Reward
Selections of behaviour appropriate for survival achieved by reward and punishment systems Motivation and avoidance In appropriate activation underline addiction
42
Model of reward circuit
Good > neural circuit that detects stimulus > neural circuit that controls behaviour > behaviour > reinforcing stimulus > reinforcing system Drugs interact with reinforcing system
43
James old (1954)
Rats implanted with stimulating electrodes in “reticular formation and hypothalamus” Rats returned to part of cage where stimulated - electrodes actually placed in medial forebrain bundle showing addictive behaviour Rewarding stimulus = reinforcement
44
Operant chamber
Rats self delivers stimulus or drug. Repeatedly stimulates medial forebrain bundle
45
Medial forebrain bundle
Has dopermenergic, seeotomergic and noritergic neurones Dopermenergic most important in reinforcement D2 dopamine antagonist blocks reinforcement (not effective as treatment in humans)
46
Reinforcing system
Dopamine axons in medial forebrain bundle that project to nucleus accumbens
47
Medial forebrain bundle
MDB is a dopamine pathway VTA to nucleus accumbens and prefrontal cortex
48
Cocaine binds with high affinity to monoamine including dopamine transporters
DA transporter knock out (germline mice) = elevated synaptic dopamine (no reputake) Cocaine normally increases motor activity by more DA in nucleus cuccumbens Cocaine administered causes no change to baseline DA or locomotion activity Still administer cocaine so other reinforcing stimulus
49
Dopamine transporter structure
12 transmembrane domain protein F105 important for high affinity cocaine binding but not for DA transport
50
Mouse knock in for mutant DA transporter
No longer bind to cocaine No elevated basal levels of DA No increase activity of locomotion So insensitive to actions of cocaine
51
Conditioned place preference test to assess reinforcing properties of cocaine
Saline area vs drug Conditioned No drug but give choice Preference for side associated with drug - wild type Knock in - don’t show rewarding effect (adverse effect)
52
Are there common mechanisms for reinforcement/addiction for other addictive drugs?
Evidence for common involvement of limbic system Evidence for common involvement of dopamine signalling especially VTA projection to nucleus accumbens Neurotransmitter - dopamine
53
Dopamine - common factor in drugs with abuse potential
Ethanol - increases DA release in nucleus accumbens DA receptor antagonists - block alcohol self administer action Opiates also increase dopamingerguc transmission in limbic system Pharmacologically different but same pathway Not adversive drugs
54
Drugs abused by humans preferentially increase synaptic dopamine concentrations in the Mesolimbic system of freely moving rats
Dose dependent (ethanol) increase in amount of dopamine in Mesolimbic system
55
Evidence for altered dopamine signalling in addiction in humans
Brain imaging PET imaging (18-fluoromethylspiroperid) to label dopamine (D2) receptors Subcortical regions - not cocaine users, 1 month off & 4 month for - degreased receptors even compared to control Age influence dopamine receptor density, cocaine users always had lower densities at any age
56
Why do users have lower levels if D2 receptors?
Cocaine increase DA levels so downrdgulation if receptors to try to bring back to normal levels Nomeostatic Compromised reward system and so craving Also seen in meth, alcohol and heroin
57
What are the long term changes associated with addiction?
Evidence - changes gene expression Eg increased DA binds to dopamine receptor causing increase in cAMP which acts on CREB (transcription factor) which gives rise to immediate early gene expression Alters lvls of receptor expression eg changes in dopamine receptors
58
Genetic basis for drug addiction
More likely to be susceptible due to genes ALDH2, D2, OPRM1
59
ALDH2
Aldehyde dehydrogenase enzyme that metabolises alcohol Alcohol via aldehyde (ADH2) to acetic acid Lower ADH2 activity, accumulates aldehyde, unpleasant (some still develop addiction but lower levels of alcohol addiction seen in pop)
60
D2 mutants
Polymorphisms Carry increase risk of alcohol and other forms of addiction
61
OPRM1
VTA opiate receptor Variants linked to addictive behaviour
62
Neuro chemical circuits in drug rewards
VTA to nucleus coecumbens in basal forebrain (involved in reward) Nucleus coecumbens to amygdala (involved in negative reinforcement)
63
Ethanol, nicotine, opiates & THC
Directly on VTA to stimulate nucleus accumbens
64
Cocaine, amphetamines, opiates and THC
Act on nucleus accumbens directly
65
Key idea
Different substances work in different parts of same circuit using different neurotransmitters but bet effect is the same - dopamine elevation downstream
66
Addiction more than just rewards
Impulsive (positive reinforcement) to compulsive (negative reinforcement) in chronic user
67
Impulsive stage
Binge intoxication > pleasurable effects > abstinence, neutral affect > crave reward repeat
68
Compulsive stage
Prolonged intoxication > relief > protracted abstinence, negative effect > relief craving repeat
69
Beyond dopamine reward circuit
Orbital frontal cortex (decision making and controlling behaviour) Higher activity in normal than addict
70
Studying alcohil dependence in rat model
Can train rats to drink with sucrose MsP alcohol preferring rats Amygdala in msp rats corticotropin releasing factor is high in dependent and alcohol preferring (most)
71
CRF
Hypothalamic hormone (neuropeptide) that acts on anterior pituitary that release acth on adrenocortex, leads to cortical release
72
CRF in amygdala may be involved in stress and genotype dependent
Rat self administers alcohol via lever. Alcohol taken out. Period of behaviour stopped. Foot shock as stressor. Increased lever press Antagonist present decreased lever press Same seen in alcohol preferring eats but greater decrease
73
Phencyclidine
Selective non competitive antagonist of NMDA receptors
74
Schizophrenia stat
Affects 1% of population Suicide number 1 cause of premature death among people with schizophrenia

Neuropharma Of CNS disorders (5 decks)

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