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For nearly three decades efforts have been made to define the role of GABAergic transmission in the mediation and perception of pain. The anatomical distribution of GABA neurons and receptors, as well as the antinociceptive responses to GABAA and GABAB receptor agonists, is consistent with the notion that manipulation of this transmitter system may be of clinical benefit in the treatment of acute, inflammatory, and neuropathic pain. Contained in this report is a review of the data in support of this proposition, a discussion of disparate and contradictory findings, and a description of theories used to explain variation in the antinociceptive responses to GABAergic drugs. Particular emphasis is placed on interpreting the results in the context of the anatomical localization and function of GABA neurons as well as the molecular and pharmacological properties of GABA receptor subtypes
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