Basic neuroscience for psychiatry — MEQ

(i) Levels and RDoC. Useful levels: molecule/receptor → synapse/plasticity → pathway → large-scale network → behaviour/syndrome. Clinical care still uses DSM/ICD categorical diagnoses for communication and eligibility. RDoC organises dimensional research constructs (e.g. negative valence, cognitive systems) across units of analysis; it does not replace clinical manuals. [4]

(ii) LTP. High-frequency or associative co-activation can strengthen synapses. At many glutamatergic synapses, NMDA receptors require glutamate and postsynaptic depolarisation to relieve Mg2+ block; Ca2+ influx engages kinases and can increase AMPA-mediated transmission. Clinical implication: learning and extinction (e.g. exposure therapy) are plasticity processes; delayed antidepressant effects have been linked to slower adaptive plasticity/neurotrophic changes rather than instantaneous 'filling a serotonin tank.' [1][6]

(iii) Dopamine map and version III. Mesolimbic — positive symptoms/salience; mesocortical — cognition/negatives; nigrostriatal — EPS with blockade; tuberoinfundibular — prolactin with blockade. Version III: multiple upstream risks converge on striatal dopamine dysregulation as a final common pathway producing aberrant salience. [2]

(iv) Methods. Structural MRI when organic red flags (atypical onset, focal signs, decline) — not to 'confirm MDD.' fMRI BOLD is a haemodynamic proxy; research-powerful; reverse inference dangerous; not routine diagnosis. [3] EEG for seizures/encephalopathy differentials. PET/SPECT occupancy underpins receptor pharmacology teaching (e.g. D2) but is not required before every prescription.

(v) Translation. Psychosis: striatal DA/aberrant salience and network dysconnectivity (triple-network framing). Depression: limbic–prefrontal and reward circuit dysfunction plus stress–neurotrophic models — not pure monoamine deficiency. Anchors: Howes–Kapur; Nestler; Menon; Logothetis for method humility. [2][5][6]