Differential distribution of metabotropic glutamate receptors 1a, 1b, and 5 in the rat spinal cord

Metabotropic glutamate receptors (mGluRs) modulate somatosensory, autonomic , and motor functions at spinal levels. mGluR postsynaptic actions over spi nal neurons display the pharmacologic characteristics of type I mGluRs; how ever, the spinal distribution of type I mGluR isoforms remains poorly defin ed. In this study, the authors describe a differential distribution of immu noreactivity to various type I mGluR isoforms (mGluR1a, mGluR5a,b, and mGlu R1b) that suggests a correlation between specific isoforms and particular a spects of spinal cord function. Two different antisera raised against mGluR 5a,b detected intense immunoreactivity within nociceptive afferent terminal fields (laminae I and II) and also in autonomic regions (parasympathetic a nd sympathetic). In contrast, two of three anti-mGluR1a antibodies did not immunostain lamina I or II. Laminae I and II immunostaining by a third anti -mGluR1a antibody Nas competed by a peptide sequence obtained from a homolo gous region in mGluR5, suggesting possible cross reactivity in fixed tissue . Autonomic neurons did not express mGluR1a immunoreactivity. All anti-mGlu R1a antibodies strongly and specifically immunolabeled dendritic and somati c membranes of neurons in the deep dorsal horn (lamina III-V) and the ventr al horn (lamina VI-IX). Somatic motoneurons expressed mGluR1a immunoreactiv ity but little or no mGluR5 immunoreactivity. Phrenic and pudendal motoneur ons expressed the highest level of mGluR1a immunoreactivity in the spinal c ord. Intense mGluR1b immunoreactivity was restricted to a few scattered neu rons and a prominent group of neurons in lamina X. Lamina II neurons expres sed low levels of mGluR1b immunoreactivity. Ultrastructurally, type I mGluR immunoreactivity was found mostly at extrasynaptic sites on the plasma mem brane, but it was also found perisynaptically, in the body of the postsynap tic regions or in relation to intracytoplasmic structures. J. Comp. Neurol. 422:464-487, 2000. (C) 2000 Wiley-Liss, Inc.