Colocalization of metabotropic glutamate receptors in rat dorsal root ganglion cells
- 13 February 2007
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 501 (5), 780-789
- https://doi.org/10.1002/cne.21285
Abstract
Glutamate is the main excitatory transmitter in both central and peripheral nervous systems. Discovery of metabotropic glutamate receptors (mGluRs) made it clear that glutamate can have excitatory or inhibitory effects on neuronal function, with group I mGluRs enhancing cell excitability but group II and III mGluRs decreasing excitability. The present study investigated the colocalization of mGluR subtypes representing groups I, II, or III in rat L5 dorsal root ganglion (DRG) cells. The analyses show that group III has the highest expression, with 75.0% of DRG cells expressing mGluR8, followed by group II, with 51.6% expressing mGluR2/3, followed by group I, with only 6.8% expressing mGluR1α. mGluR8 is expressed by small, medium, and large diameter cells. In contrast, mGluR1α and mGluR2/3 are expressed by mainly small and medium cells. Approximately half of cells expressing group I mGluR1α also express either group II mGluR2/3 or group III mGluR8. These mGluR1α double-labeled populations are not likely to overlap since >1.0% of mGluR1α are triple-labeled. As expected from the high percentage of single-labeled mGluR2/3 and mGluR8 cells, there is a considerable population of double-labeled cells with ≈30% of each population expressing both receptors. Due to the fact that the number of mGluR1α-expressing cells in the DRG is low, the percentage of triple-labeled cells is also low (≈1–2%). The prevalence of groups II and III indicate that glutamate could have a substantial inhibitory effect of primary afferent function, reducing and/or fine-tuning sensory input before transmission to the spinal cord. These anatomical data highlight the potential inhibitory role glutamate may play in peripheral sensory transmission. J. Comp. Neurol. 501:780–789, 2007.Keywords
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