Biological and Clinical Neurosciences Relevant to Psychiatry
Core neuroscience for psychiatry
A candidate must map neurotransmitter systems to clinical effects. Dopamine pathways: mesolimbic (reward, positive symptoms), mesocortical (negative and cognitive symptoms), nigrostriatal (movement), and tuberoinfundibular (prolactin). Serotonin influences mood, anxiety, sleep, appetite, and GI motility; norepinephrine drives arousal and autonomic tone; GABA and glutamate are the major inhibitory and excitatory systems; acetylcholine matters for memory and anticholinergic burden. Know the HPA axis and cortisol feedback, because chronic stress and depression questions often hinge on it. Neuroanatomy should be symptom-based: prefrontal cortex (executive function, impulse control), amygdala (fear, threat detection), hippocampus (memory, stress regulation), basal ganglia (movement, OCD circuitry), thalamus (sensory relay). Genetics is polygenic and probabilistic; heritability is not determinism, and CYP2D6/2C19 pharmacogenomics changes exposure, not guaranteed response. Neuroimaging is mostly research or rule-out, not diagnostic for primary psychiatric disorders. Sleep architecture and EEG basics appear in delirium and seizure differentials. Traps: assuming schizophrenia is purely dopaminergic; confusing serotonin syndrome with neuroleptic malignant syndrome; treating a pharmacogenomic report as a prescribing mandate; forgetting medical mimics such as thyroid disease, B12 deficiency, or delirium. Worked example: a patient on haloperidol develops galactorrhea and amenorrhea. Map this to tuberoinfundibular dopamine blockade releasing prolactin, not to a serotonin effect. Rule of thumb: link each receptor or pathway to one predictable adverse effect, and check the medical differential before attributing symptoms to psychiatry.