Nociceptive regulation of GABA(B) receptor gene expression in rat spinal cord

Activation of gamma-aminobutyric acid (GABA) neurotransmission evokes antin ociceptive responses in laboratory animals. The recent cloning of GABA(B) r eceptor gene products makes it possible to examine the regulation of this r eceptor system as it relates to the mediation of pain-related sensory infor mation. Inasmuch as acute and chronic pain alter the expression of a number of nociception-related receptors, and because such changes are important c omponents in the regulation of pain, the present study was undertaken to de termine whether GABA(B) receptor gene expression is altered in sensory syst ems following a peripheral nociceptive stimulus. Solution hybridization-nuc lease protection assays conducted 24 h after formalin injection into the ri ght hindpaw of the rat revealed a significant bilateral increase in GABA(B) R1 and R2 receptor expression in the dorsal lumbar spinal cord, and a sign ificant increase ih GABA(B) R1 receptor mRNA in the ipsilateral lumbar dors al root ganglion. These findings indicate an activity-dependent, differenti al regulation of GABA(B) R1 and R2 receptor gene expression in spinal senso ry systems in response to chemogenic nociceptive activation, suggesting tha t GABA(B) receptor plasticity may play an important role in regulating the mediation, and perception, of chronic pain. (C) 1999 Elsevier Science Ltd. All rights reserved.