Expression of metabotropic glutamate receptors mRNA in the thalamus and brainstem of monoarthritic rats
Evidence for the involvement of metabotropic glutamate receptors (mGluR) in sensory processing has been emerging. Additionally, the differential distribution of distinct mGluR subtypes mRNA in particular thalamic nuclei of normal rats suggests that they could be involved in the processing of somatos...
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Veröffentlicht in: | Brain research. Molecular brain research. 2000-09, Vol.81 (1), p.140-154 |
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Sprache: | eng |
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Zusammenfassung: | Evidence for the involvement of metabotropic glutamate receptors (mGluR) in sensory processing has been emerging. Additionally, the differential distribution of distinct mGluR subtypes mRNA in particular thalamic nuclei of normal rats suggests that they could be involved in the processing of somatosensory information. In the present study, mGluR1, 3, 4 and 7 mRNAs expression was investigated by in situ hybridisation in selected brainstem and thalamic nuclei of adult monoarthritic rats at different time points of the disease (2, 4 and 14 days). Monoarthritic rats displayed behavioural and physical signs of painful arthritis at all time points. At 2 days of monoarthritis the mGluR1 mRNA expression was decreased mainly in the ventrobasal complex (VB) and in the posterior thalamic nuclei (Po) contralateral to the inflamed joint. The mGluR4 mRNA expression was also reduced, but minimum values were found at 4 days of monoarthritis, when no changes could be found in mGluR1 mRNA expression. At 14 days, mGluR4 mRNA expression was similar to controls, while mGluR1 mRNA was again reduced. Similar decreases of mGluR7 mRNA expression in the VB and Po were found at all time points, while mGluR3 mRNA expression was bilaterally increased in the reticular thalamic nucleus (Rt). In the brainstem no changes could be found in the expression of any mGluR subtype mRNA. The reduced expression of mGluR1, 4 and 7 transcripts in VB and Po, and the increases of mGluR3 mRNA in the Rt may contribute to counteract the increased noxious input arising from the periphery. |
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ISSN: | 0169-328X 1872-6941 |
DOI: | 10.1016/S0169-328X(00)00176-5 |