Key neurotransmitters and their actions

Overview

Key neurotransmitters (dopamine, serotonin, noradrenaline, GABA, glutamate, acetylcholine, and opioid peptides) each have characteristic receptor systems and physiological roles - understanding these systems explains both the therapeutic mechanism and characteristic adverse effect profile of psychotropic and other centrally-acting drugs discussed throughout pharmacology
Foundational neuropharmacology underlying understanding of antidepressants, antipsychotics, anxiolytics, and substances of misuse discussed throughout this specialty

Dopamine (reward, motor control, and specific psychiatric symptom domains) - excess implicated in psychosis, deficiency in Parkinson disease and addiction's reward pathway dysregulation; serotonin (mood, anxiety, GI motility) - the target of SSRIs, with excess causing serotonin syndrome; GABA (the primary inhibitory neurotransmitter) - potentiated by benzodiazepines and alcohol, with abrupt withdrawal from chronic potentiation causing the CNS hyperexcitability of withdrawal syndromes; glutamate (the primary excitatory neurotransmitter) - counterbalances GABA, with dysregulation implicated in withdrawal state hyperexcitability and some neurotoxic mechanisms

Not directly tested via a specific investigation, but understanding a drug's primary neurotransmitter target explains both its therapeutic use and predictable interaction/adverse effect risk with other drugs acting on the same or a related system
Mechanism-based understanding of neurotransmitter systems explains why combining drugs acting on the same system (e.g. multiple serotonergic agents) increases risk of an exaggerated effect (serotonin syndrome), while drugs acting on opposing systems (e.g. GABA potentiation withdrawal countered by benzodiazepine replacement) explains rational withdrawal management strategy

GABA-glutamate balance and withdrawal syndrome hyperexcitability (alcohol, benzodiazepine withdrawal), dopamine dysregulation in psychosis and addiction, serotonin syndrome from combined serotonergic drug exposure, acetylcholine and the cholinergic/anticholinergic toxidrome pair
Chronic alcohol or benzodiazepine use potentiates GABA (inhibitory) and suppresses glutamate (excitatory) signalling - abrupt cessation removes this suppression, causing unopposed glutamate-driven CNS hyperexcitability that directly explains withdrawal syndrome features (tremor, seizures, autonomic hyperactivity), and why benzodiazepines (restoring GABA potentiation) are the standard withdrawal treatment for both substances despite treating withdrawal from either one

3 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.