Abuse Potential of Soma: the GABA(A) Receptor as a Target

Abstract

Soma(®) (carisoprodol) is an increasingly abused, centrally-acting muscle relaxant. Despite the prevalence of carisoprodol abuse, its mechanism of action remains unclear. Its sedative effects, which contribute to its therapeutic and recreational use, are generally attributed to the actions of its primary metabolite, meprobamate, at GABA(A) receptors (GABA(A)R). Meprobamate is a controlled substance at the federal level; ironically, carisoprodol is not currently classified as such. Using behavioral and molecular pharmacological approaches, we recently demonstrated carisoprodol, itself, is capable of modulating GABA(A)R function in a manner similar to central nervous system depressants. Its functional similarities with this highly addictive class of drugs may contribute to the abuse potential of carisoprodol. The site of action of carisoprodol has not been identified; based on our studies, interaction with benzodiazepine or barbiturate sites is unlikely. These recent findings, when coupled with numerous reports in the literature, support the contention that the non-controlled status of carisoprodol should be reevaluated.

Figure 1. Chemical structures of carisoprodol and meprobamate

Carisoprodol and meprobamate are propanediol dicarbamates. Carisoprodol was synthesized by replacing a hydrogen on a carbamyl nitrogen of meprobamate with an isopropyl group. Chemical structures were obtained from PubChem, an online resource made available through the United States National Library of Medicine (http://pubchem.ncbi.nlm.nih.gov.).