Modification of GABA_B1 and GABA_B2 receptor subunits in the somatosensory cerebral cortex and thalamus of rats with absence seizures (GAERS)
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Colleges, School and Institutes
In the present study, we have investigated GABA(B) receptor expression in somatosensory cortex (SI) and the ventrobasal (VB) and reticular (Rt) thalamic nuclei of Genetic Absence Epilepsy Rats from Strasbourg (GAERS), which represent an animal model for the human absence epilepsy. We focused our attention oil the thalamocortical network because it has been demonstrated that absence seizures are generated in this specific circuit, which is under the control of several inhibitory, e.g. GABA, and excitatory systems. Autoradiography data obtained with the GABA(B) receptor antagonist \H-3\CGP62349 did not show any differences in K-d or B-max values between control rats and GAERS. In situ hybridisation (ISH) results showed a significant increase in messenger RNA for GABA(B1) in the SI and a decrease in the VB thalamic nucleus but not in the R1 thalamic nucleus. By contrast the immunocytochemical data revealed an increased expression of both GABA(B1) and GABA(B2) receptor subunits in all the regions examined. somatosensory cerebral cortex. VB thalamus and Rt nucleus fit GAERS compared to controls. The main finding was an up-regulation of GABA(B) receptor protein in the corticothalmic circuit in GAERS compared to Controls. (C) 2003 Elsevier B.V. All rights reserved.
|Number of pages||13|
|Publication status||Published - 1 Jul 2003|
- somatosensory system, immunohistochemistry, generalised seizures, thalamocortical circuit, binding studies, in situ hybridisation, typical absence