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CNS Drugs Mechanisms

BS2014 Neuroscience Drug Targets in CNS and proposed mechanisms

Drug Category Function
Tricyclic Antidepressant - e.g. doxepine Inhibits re-uptake of NA or 5-HT
SSRIs (Antidepressants) - e.g. Prozac Selective serotonin re-uptake inhibitor
Irreversible MAOIs (Antidepressants) - e.g. phenelzine Inhibit metabolism of NA by monoamine oxidase inhibition (MAOI)
α-2 adrenoceptor antagonists (antidepressants) - e.g. mirtrazapine Enhance release of NA into synaptic cleft by inhibiting negative-feedback inhibition of NA release as triggered by binding of NA to pre-synatptic α-2 adrenoceptors (autoreceptors)
Manic symptoms (bipolar disorder); Lithium compounds - e.g. Lithium citrate Interfer with inositol recycling by inhibiting inositol monophosphate. Impacts a major (Gαq) pathway.
Stimulant; Amphetamine Sympathomimetic- competes for Uptake 1 and inhibits MOA; prevents NA removal from synaptic cleft.
Stimmulant; Cocaine Sympathomimetic - competes with NA for Uptake 1
Anti-epileptics (AED)- e.g. phenytoin Selectively block most active Na+ channels to inhibit the depolarisation.
Schizophrenia Antipsychotics - e.g. Haloperidol D2 (dopamine receptor) antagonist (atypical)
Schizophrenia Antipsychotic - e.g. Clozapine 5-HT 2A/2C (serotonin)receptor antagonist (atypical)
Schizophrenia Antipsychotic - e.g. mGluR 2/3 agonist (clinical trials) Inhibits glutamate release into synaptic cleft
Opioid Analgesics - e.g. morphine Opioid GPCR agonist = primarily μ, Gαi; βγ subunit activity on Na+ (deactivation- decreased influx), K+ (activation/ increased efflux) and Ca2+ (downregulated - decreased vesicular exocytosis conductance) - decreased neural excitability
Created by: Kingfisher
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