Up-regulation of metabotropic glutamate receptor 3 mRNA expression in the cerebral cortex of monoarthritic rats

Citation
Fl. Neto et al., Up-regulation of metabotropic glutamate receptor 3 mRNA expression in the cerebral cortex of monoarthritic rats, J NEUROSC R, 63(4), 2001, pp. 356-367
Citations number
65
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE RESEARCH
ISSN journal
03604012 → ACNP
Volume
63
Issue
4
Year of publication
2001
Pages
356 - 367
Database
ISI
SICI code
0360-4012(20010215)63:4<356:UOMGR3>2.0.ZU;2-8
Abstract
Metabotropic glutamate receptors (mGluR) have been shown to play a role in the modulation of acute and inflammatory pain. Additionally, we have recent ly detected time-dependent changes in the mRNA expression of several mGluR subtypes in thalamic nuclei of monoarthritic (MA) rats. In the present stud y, mGluR1, -3, -4, and -7 subtype mRNA expression was analyzed by in situ h ybridization with radioactively labelled oligonucleotide probes in cerebral cortical regions of normal and MA rats at 2, 4, and 14 days of the disease . The mGluR1, -4, and -7 mRNAs were at background level in normal rats and did not change in MA animals. In contrast, mGluR3 mRNA expression was abund ant in normal rats and was significantly increased in cortical areas of MA rats at all time points. Higher changes were detected bilaterally at 4 days , predominantly in layers IV/V, in the motor, primary, and secondary somato sensory cortices (average increases of 50-75%), but maximum rises occurred in the contralateral cingulate cortex (+138%), No changes were detected in the auditory cortex. The present data show an up-regulation of mGluR3 mRNA expression in the motor, somatosensory, and limbic cortices of MA rats, Thi s possibly reflects the occurrence of central mechanisms counteracting the increased transmission of nociceptive input arising from the inflamed paw a nd the impaired motor behavior of these rats. Changes in the cingulate cort ex may be related to the motivational-affective component of nociception. ( C) 2001 Wiley-Liss, Inc.