In Generalized Anxiety Disorder (GAD), which neurotransmitter imbalance and corresponding mechanism explains the efficacy of pregabalin?

• A Serotonin deficiency; pregabalin is a 5-HT1A partial agonist
• B Excess norepinephrine; pregabalin blocks beta-1 adrenergic receptors
• C Excess excitatory amino acid release; pregabalin binds alpha-2-delta subunit of voltage-gated calcium channels reducing glutamate release ✓
• D GABA deficiency; pregabalin is a GABA-A receptor positive allosteric modulator

Explanation

Pregabalin binds to the alpha-2-delta subunit of presynaptic voltage-gated calcium channels, reducing calcium influx and thereby reducing the release of excitatory neurotransmitters (glutamate, norepinephrine, substance P). Despite its structural resemblance to GABA, pregabalin does NOT bind GABA receptors or enhance GABAergic transmission directly. It is approved for GAD in Europe (though not FDA-approved for GAD). Buspirone is a 5-HT1A partial agonist used in GAD. SSRIs/SNRIs act on serotonin/norepinephrine transporters.

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

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