Spinal cord injury (SCI) initiates biochemical events that lead to an incre
ase in extracellular excitatory amino acid concentrations, resulting in glu
tamate receptor-mediated excitotoxic events. These receptors include the th
ree groups of metabotropic glutamate receptors (mGluRs). Group I mGluR acti
vation can initiate a number of intracellular pathways that increase neuron
al excitability. Group II and III mGluRs may function as autoreceptors to m
odulate neurotransmission. Thus, all three groups may contribute to the mec
hanisms of central sensitization and chronic central pain. To begin evaluat
ing mGluRs in SCI, we quantified the changes in mGluR expression after SCI
in control (naive), sham, and impact injured adult male Sprague-Dawley rats
(200-250 g). SCI was produced at spinal segment TIO with a New York Univer
sity impactor (12.5-mm drop, 10-g rod of 2-mm diameter). Expression levels
were determined by Western blot and immunohistochemistry analyses at the ep
icenter of injury, as well as segments rostral and caudal. The group I subt
ype mGluR1 was increased over control levels in segments rostral and caudal
by postsurgical day (PSD) 7 and remained elevated through PSD 60. The grou
p I subtype mGluR5 was unchanged in all segments rostral and caudal to the
injury at every time point measured. Group Il mGluRs were decreased compare
d to control levels from PSD 7 through PSD 60 in all segments. These result
s suggest that different subtypes of mGluRs have different spatial and temp
oral expression patterns following SCI. The expression changes in mGluRs pa
rallel the development of mechanical allodynia and thermal hyperalgesia fol
lowing SCI; therefore, understanding the expression of mGluRs after SCI may
give insight into mechanisms underlying the development of chronic central
pain. (C) 2001 Academic Press.