Neurotransmitters and psychotropic targets (MEQ)

(i) Slogan correction. Depression is not established as simple low serotonin; monoamine history is important, but biomarker support for a pure serotonin-deficiency theory is inconsistent — still, antidepressants have efficacy evidence. Psychosis is not “high dopamine everywhere”: Howes/Kapur version III emphasises striatal dopamine dysregulation as a final common pathway; teach four pathways so mesolimbic efficacy is not confused with nigrostriatal EPS or tuberoinfundibular prolactin.[1][2][6]

(ii) Target map. SSRI → SERT; SNRI → SERT+NET; mirtazapine → alpha-2 antagonism with 5-HT2/3 antagonism; FGA → high D2 antagonism; SGA → D2 ± 5-HT2A multi-receptor profiles; BZD → GABA-A positive allosteric modulation; ketamine pathway → NMDA-related cascades and synaptic plasticity signalling rather than monoamine reuptake.[3][6]

(iii) Delayed onset. Acute SERT blockade is initiation; clinical response tracks adaptive intracellular and network changes over weeks (Hyman–Nestler). Do not say levels take weeks to rise.[3][6]

(iv) Toxidromes. Serotonin toxicity: excess 5-HT tone; clonus/hyperreflexia; serotonergic drug context; Hunter criteria. NMS: relative dopamine hypofunction with antipsychotic context; rigidity, slower evolution, often bradyreflexia — different mechanism language and management priorities (stop serotonergic agents vs stop dopamine antagonists).[4]

(v) Muscarinic implication. Xanomeline-trospium efficacy shows antipsychotic benefit can be achieved via M1/M4-preferring muscarinic agonism without classical D2 blockade as the primary mechanism — exams now expect multi-system maps, not D2-only dogma.[5]