In the vertebrate brain, the thalamus serves as a relay and integration station for diverse neuronal information en route from the periphery to the cortex. Deficiency of TH during development results in severe cerebral abnormalities similar to those seen in the mouse when the retinoic acid receptor (ROR)α gene is disrupted. To investigate the effect of the thyroid hormone receptors (TRs) on RORα gene expression, we used intact male mice, in which the genes encoding the α and β TRs have been deleted. In situ hybridization for RORα mRNA revealed that this gene is expressed in specific areas of the brain including the thalamus, pons, cerebellum, cortex, and hippocampus. Our quantitative data showed differences in RORα mRNA expression in different subthalamic nuclei between wild-type and knockout mice. For example, the centromedial nucleus of the thalamus, which plays a role in mediating nociceptive and visceral information from the brainstem to the basal ganglia and cortical regions, has less expression of RORα mRNA in the knockout mice (-37%) compared to the wild-type controls. Also, in the dorsal geniculate (+72%) and lateral posterior nuclei (+58%) we found more RORα mRNA in dKO as compared to dWT animals. Such differences in RORα mRNA expression may play a role in the behavioral alterations resulting from congenital hypothyroidism.
|Number of pages||8|
|Publication status||Published - Feb 2005|
- Orphan receptor
- Retinoid-related receptor
- Thyroid hormone