That's the full neuroscience breakdown. Here's a quick orientation of what was covered:
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Schizophrenia — The three dopamine pathway model (mesolimbic D2 hyperactivity → positive symptoms; mesocortical D1 hypoactivity → negative symptoms; nigrostriatal → side effects). Upstream driver: NMDA receptor hypofunction on PV+ GABAergic interneurons disinhibiting glutamate, which drives the dopamine imbalance. Plus the 5-HT2A serotonin arm and why second-gen antipsychotics block both D2 and 5-HT2A.
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Depression — Five converging levels: monoamine hypothesis (5-HT1A, α2 autoreceptors), HPA axis (cortisol/GR-mediated hippocampal atrophy), neurotrophic hypothesis (BDNF→TrkB→CREB cascade), glutamate/ketamine rapid synaptogenesis via AMPA/mTOR, and neuroinflammation (IDO → kynurenine → quinolinic acid as an NMDA agonist).
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Bipolar — Kindling/anticonvulsant model; CACNA1C (L-type Ca²⁺ channel) as the top genetic hit; lithium's molecular targets (IMPase inhibition, GSK-3β inhibition, PKC, BDNF upregulation); circadian clock gene disruption.
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Anxiety — Amygdala-centered circuit + CSTC worry loop; GABA-A receptor PAM mechanism of benzodiazepines (α1 = sedation, α2/α3 = anxiolysis); α2δ VSCCs for pregabalin; CRH-R1 in amygdala; NE locus coeruleus hyperreactivity.
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Panic — LC NE storm (α1/α2/β receptors); parabrachial nucleus/suffocation alarm; CO2 hypersensitivity via amygdala ASICs; CCK-B receptors; why SSRIs take weeks to work (5-HT1A autoreceptor desensitization).
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PTSD — Fear conditioning (NMDA/AMPA LTP in lateral amygdala); vmPFC extinction failure; hippocampal atrophy and context failure; paradoxically low cortisol with hypersensitive GR; high CRH and NE; why prazosin, propranolol, and MDMA-assisted therapy work at the receptor level.
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Eating Disorders — Hypothalamic ARC: NPY/AgRP (hunger) vs POMC/α-MSH (satiety) acting at MC4R; ghrelin (GHSR1a) and leptin (JAK/STAT); 5-HT2C for SSRIs in bulimia; mesolimbic D2 hypersensitivity and aberrant reward in anorexia; insula interoception.
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BPD — Amygdala hyperreactivity + PFC hypofunction; serotonin impulsivity axis (5-HIAA ↓); µ-opioid system and social pain (naltrexone rationale); HPA epigenetic changes (GR methylation from childhood trauma); NE storms and dissociation.