The differential expression of 16 NMDA and non-NMDA receptor subunits in the rat spinal cord and in periaqueductal gray.

Diverse arrays of glutamate-gated channels in the spinal cord and associated pathways are partly responsible for sensory input, for altered sensitivity to peripheral stimuli during inflammation, and for generation of motor patterns. The expression of 16 genes, encoding all known subunits for the NMDA receptor (NR1, NR2A to NR2D), AMPA/low-affinity kainate (GluR-A to -D), high-affinity kainate ionotropic receptors (KA-1, -2, GluR-5 to -7) and two orphan receptor subunits (delta-1 and -2) was examined by in situ hybridization in rat lumbar spinal cord, and in the periaqueductal gray. Subunit mRNAs for GluR-A, -B Flip, KA-2, and NR1 were abundant in the dorsal horn, with NR2D lightly expressed. Occasional cells in lamina II contained NR2C mRNA. While the GluR-A gene was preferentially expressed in laminae I and II-outer, GluR-B mRNA was evenly expressed throughout all superficial laminae (I, II-outer, II-inner, and III). Large neurons in laminae IV and V expressed mainly NR1, GluR-C, and to lesser extents the GluR-B, GluR-D, and NR2D genes. Lamina I contained occasional cells expressing the GluR-5 gene, whereas GluR-7 mRNA was present in scattered cells in all superficial laminae. In motor neurons, GluR-B Flip, -C Flip, -D Flip, and NR1 mRNAs were expressed heavily, and those of NR2D and KA-1 weakly. Possibly connected to the RNA editing mechanism, GluR-B was the only subunit whose RNA was concentrated in motor neuron cell nuclei in addition to the cytoplasm. delta-1 and -2 mRNAs were found at low levels throughout the gray matter. NR2A, NR2B, and GluR-6 mRNAs were undetectable. For the periaqueductal gray, prominent mRNAs were GluR-A, -B, and NR1. An en passant observation concerned high levels of NR2C mRNA in the pineal gland.