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Differential Regulation of GABAB Receptor Subunit Expression and Function

The GABAB receptor is a G protein-coupled heterodimer composed of GABAB1 and GABAB2 subunits. In the present study, experiments were undertaken to examine the relationship between GABAB receptor function and subunit expression in the rat lumbar spinal cord following pharmacological and physiological manipulation of this receptor system. Although formalin-induced hind paw inflammation increases the production of GABAB1 and GABAB2 protein in the spinal cord within 24 h, there is no change in receptor function, as measured by the baclofen-stimulated guanosine 5′-O-(3-[35S]thiotriphosphate) ([35S]GTPγS) binding assay. Conversely, although chronic (7 days) administration of baclofen, a GABABreceptor agonist, abolishes baclofen-stimulated [35S]GTPγS binding in the spinal cord tissue, causes tolerance to the sedative and antinociceptive effects of the drug, increases the number of formalin-induced hind paw flinches, and induces mechanical hyperalgesia, this treatment had no effect on the levels of GABAB1 or GABAB2 mRNAs in the lumbar spinal cord. The results indicate a lack of concordance between expression of GABAB1 and GABAB2 subunits and GABAB receptor function, suggesting these subunit proteins may serve multiple functions in the cells. Moreover, these findings indicate that nongenomic mechanisms are primarily responsible for the GABAB receptor desensitization that occurs during prolonged exposure to receptor agonist.