Basic neuroscience for psychiatry — structured clinical viva

Multilevel answer. Genes, development, substance hits, and stress can converge on synaptic and circuit dysfunction expressed as a clinical syndrome — not a single litre of wrong chemical. [1][5]

Psychosis model. Dopamine hypothesis version III: final common pathway of striatal dopamine dysregulation and aberrant salience; imaging supports increased dopaminergic occupancy/tone in samples. Cannabis is an upstream risk, not proof of one mechanism alone. [1][2]

Pathways. Teach mesolimbic (positive symptoms), mesocortical (cognition/negatives), nigrostriatal (EPS), tuberoinfundibular (prolactin). [1]

Scans. MRI if red flags; normal MRI does not exclude primary psychosis. fMRI BOLD is research haemodynamics, not a diagnostic photo of 'the imbalance.' [6] EEG if seizure/encephalopathy concerns.

Ketamine dual lesson. Psychotomimetic NMDA antagonism supports glutamate models; separate literature shows rapid antidepressant effects in treatment-resistant depression protocols — different clinical contexts. [3][4]

Depression contrast. Multilevel circuit and molecular dysfunction, stress–neurotrophic themes; reject pure serotonin deficiency monologue. [5]

Communication. 'Brain systems involved in meaning, motivation and perception are disrupted; medicines that modulate dopamine can reduce positive symptoms; recovery also needs psychosocial care; we do not diagnose this with a routine colour brain scan.' [1][6]