GABAB2 receptor subunit mRNA decreases in the thalamus of monoarthritic animals

Many studies have implicated GABAB receptors in pain transmission mechanisms, especially in the spinal cord. In the thalamus, mRNA expression of the GABAB(1b) isoform was shown to be regulated in relay nuclei in response to chronic noxious input arising from experimental monoarthritis. GABAB(1a) and GABAB2 mRNA expression was here determined by in situ hybridisation in the brain of control, 2, 4, 7 and 14 days monoarthritic rats, to evaluate whether this expression was regulated by chronic noxious input in thalamic nuclei. mRNA labelling was analysed quantitatively in the ventrobasal complex, posterior, central medial/central lateral and reticular thalamic nuclei; the thalamic visual relay and dentate gyrus were examined for control. No mRNA expression was detected for GABAB(1a) in control and monoarthritic animals. Similarly, GABAB2 mRNA was not found in the reticular nucleus. However, GABAB2 mRNA expression was observed in the ventrobasal complex, posterior and central medial/central lateral nuclei of control animals. A significant decrease of 42% at 2 days and 27% at 4 days of monoarthritis was observed in the ventrobasal complex contralaterally, when compared with controls, returning to basal levels at 7 days of monoarthritis. In the ipsilateral posterior nucleus, there was a significant decrease of 38% at 2 days of monoarthritis. No significant changes were observed in central medial/central lateral nuclei. The data suggest that GABAB2 mRNA expression in the ventrobasal complex and posterior nucleus is regulated by noxious input and that GABAB receptors might play a role in the plasticity of these relay nuclei during chronic inflammatory pain.