The neurochemistry of drug reward

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  • Created by: The Shrew
  • Created on: 19-05-16 18:06
Morphine reduces activity
of the outer cortex
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Cocaine increases activity
of the whole brain
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Psychoactive drugs
Influence subjective experience and behaviour by acting on the nervous system
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Oral ingestion
Swallow and dissolve in fluid of stomach and carried into intestine where its absorbed and goes into bloodstream
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Alcohol doesn't have a receptor but
Is very soluble in fat- passes through stomach wall almost immediately
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3 types of injection
Subcutaneous- fat under skin/ intramuscular- muscle/ intravenous- vien- quick- can't counteract effects
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Absorbed into bloodstream through capillaries in lungs
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Absorbtion through mucus membranes
Cocaine through nasal membranes damages them through vasoconstriction
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Crossing blood-brain barrier depends on
Liposolubility- more soluble, more addictive
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USA Schedule I, II, III
Schedule I= just used for abuse, II= some medical use, III= used a lot in medicine
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UK based on
Seriousness of punishment
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Limbic system- Nigostratial pathway
For movement to basal ganglia
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Mesolimbic pathway
Reward system linked to nucleus accumbens
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Mesocortical tract
Secretion of drug linked to nucleus accumbens
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Dopamine pathways- Nigostratiatal pathway
Substantia nigra neurones projecting to dorsal stratium
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Degenerates in
Parkinson's disease
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Mesocorticolimbic system
VTA neurones project to cortical and limbic sites, including the nucleus accumbens
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All drugs of abuse
flood system with dopamine
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Specific dopamine antagonistic drugs
Dopamine blocked- get no rewards= depression/ parkinsons disease/ antipsychotics do this a bit
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Antagonist drug decreases
Break point
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PET replacement
Dopamine increases in nucleus accumbens= desensitization- overall dopamine function is diminished- less natural production, need more of the drug
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Interfere with
Diffusion, reuptake, glial reuptake, enzymatic breakdown, NT remain longer in the synaptic cleft
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Dopamine transport
moves NT back into the terminal
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More NT in synapse
continuous stimulation
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Amphetamine increases concentration of dopamine in synaptic cleft in 4 ways- 1)
Binds to presynaptic membrane of dopaminergic neurones to induce release of dopamine
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Interacts with dopamine containing synaptic vesicles, releasing free dopamine into nerve terminal
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Binds to monoamine oxidase in dopaminergic neurones and prevents degradation of dopamine, leaving free dopamine in nerve terminal
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Binds to dopamine re-uptake transporter causing it to act in reverse and transport free dopamine out of the nerve terminal
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developed from amphetamine but more gets in brain, longer lasting, more harmful to CNS
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Inhibit release of GABA from nerve terminal, reducing inhibitory effect of GABA on dopaminergic neurones
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Liking down to
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Bind to CBI receptors which activates G-proteins that activate/ inhibit a number of signal transduction pathways (including GABA)
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Drugs that act on serotonin system
Hallucinagens/ ecstacy- Less addictive
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Hallucinogens structurally resemble serotonin
Affect serotonin receptors- take away perception filters- experience loads more
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Block reuptake of serotonin
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Increases serotonin released in synapse- acts on serotonin transporter and is transported to nerve terminal= release of serotonin/ Within the terminal, MDMA interferes with the storage of serotonin within the vesticles and increases the amount releas
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Can also enhance release of
Dopamine and noradrenalin
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Can also inhibit
Monoamine reuptake and delay metabolism by inhibition of monoamine oxidase
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Alcohol, Tranquillizers
Inhibits GABA
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Stimulates neurones
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Can over stimulate
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Phencyclidine- developed
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Metabolic tolerance
Less drug getting into site of action- liver increases production of enzyme alcohol dehydrogenase
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Functional tolerance
decrease in responsiveness at site of action, fewer receptors, decreased efficiency of binding at receptors
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Card 2


Cocaine increases activity


of the whole brain

Card 3


Psychoactive drugs


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Card 4


Oral ingestion


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Card 5


Alcohol doesn't have a receptor but


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