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GABA(B2) receptor subunit mRNA decreases in the thalamus of monoarthritic animals
Joana Ferreira-Gomes1, Fani L Neto, José M Castro-Lopes
1Institute of Histology and Embryology, Faculty of Medicine and IBMC, 4200-319 Porto, University of Porto, Portugal.
Abstract:
Many studies have implicated GABA(B) receptors in pain transmission mechanisms, especially in the spinal cord. In the thalamus, mRNA expression of the GABA(B(1b)) isoform was shown to be regulated in relay nuclei in response to chronic noxious input arising from experimental monoarthritis. GABA(B(1a)) and GABA(B2) 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 GABA(B(1a)) in control and monoarthritic animals. Similarly, GABA(B2) mRNA was not found in the reticular nucleus. However, GABA(B2) 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 GABA(B2) mRNA expression in the ventrobasal complex and posterior nucleus is regulated by noxious input and that GABA(B) receptors might play a role in the plasticity of these relay nuclei during chronic inflammatory pain.
Insights
This study found that GABA(B2) mRNA expression in specific thalamic nuclei decreases during chronic inflammatory pain in rats. This suggests GABA(B) receptors are involved in pain processing and thalamic plasticity.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- GABA(B) receptors are implicated in pain pathways, particularly in the spinal cord.
- Previous research showed GABA(B(1b)) mRNA regulation in thalamic relay nuclei due to chronic pain.
- The role of other GABA(B) isoforms in thalamic pain processing remained unclear.
Purpose of the Study:
- To investigate the mRNA expression of GABA(B(1a)) and GABA(B2) isoforms in rat thalamic nuclei during experimental monoarthritis.
- To determine if this expression is modulated by chronic noxious input in specific thalamic nuclei.
Main Methods:
- In situ hybridization was used to quantify GABA(B(1a)) and GABA(B2) mRNA expression in control and monoarthritic rat brains.
- Analysis focused on ventrobasal complex, posterior, central medial/central lateral, and reticular thalamic nuclei.
- Quantitative analysis compared mRNA labeling between control and various time points (2, 4, 7, 14 days) of monoarthritis.
Main Results:
- GABA(B(1a)) mRNA was not detected in any thalamic nuclei studied, in both control and monoarthritic rats.
- GABA(B2) mRNA was absent in the reticular nucleus but present in the ventrobasal complex, posterior, and central medial/central lateral nuclei of control rats.
- A significant decrease in GABA(B2) mRNA was observed in the contralateral ventrobasal complex (42% at 2 days, 27% at 4 days) and ipsilateral posterior nucleus (38% at 2 days) during monoarthritis, returning to baseline by 7 days.
Conclusions:
- GABA(B2) mRNA expression in the ventrobasal complex and posterior nucleus is regulated by noxious input associated with chronic inflammatory pain.
- These findings suggest that GABA(B) receptors play a role in the neural plasticity of thalamic relay nuclei during chronic pain conditions.
