Activation of
gamma-aminobutyric acid (
GABA) neurotransmission evokes antinociceptive responses in laboratory animals. The recent cloning of
GABA(B) receptor gene products makes it possible to examine the regulation of this receptor system as it relates to the mediation of
pain-related sensory information. Inasmuch as acute and
chronic pain alter the expression of a number of nociception-related receptors, and because such changes are important components in the regulation of
pain, the present study was undertaken to determine whether
GABA(B) receptor gene expression is altered in sensory systems following a peripheral nociceptive stimulus.
Solution hybridization-nuclease protection assays conducted 24 h after
formalin injection into the right 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 significant increase in
GABA(B) R1 receptor mRNA in the ipsilateral lumbar dorsal root ganglion. These findings indicate an activity-dependent, differential regulation of
GABA(B) R1 and R2 receptor gene expression in spinal sensory systems in response to chemogenic nociceptive activation, suggesting that
GABA(B) receptor plasticity may play an important role in regulating the mediation, and perception, of
chronic pain.