Buspirone's anxiolytic mechanism in Generalised Anxiety Disorder is distinct from benzodiazepines because it:

• A Enhances GABA-A chloride channel opening frequency
• B Blocks reuptake of serotonin and norepinephrine in the locus coeruleus
• C Inhibits monoamine oxidase type A in the raphe nuclei
• D Acts as a partial 5-HT1A agonist at presynaptic raphe nuclei and postsynaptic limbic neurons with no GABA activity ✓

Explanation

Buspirone is a selective partial 5-HT1A agonist. At presynaptic somatodendritic autoreceptors on raphe neurons it acts as a full agonist, reducing raphe neuronal firing and serotonin release. At postsynaptic 5-HT1A receptors in the hippocampus and frontal cortex it acts as a partial agonist, producing anxiolysis. Crucially, buspirone has no affinity for GABA-A or benzodiazepine receptors, explaining its lack of sedation, muscle relaxation, anticonvulsant effect, or abuse potential. Its delayed onset (2–4 weeks) reflects neuroadaptive changes rather than acute GABAergic modulation.

Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.

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