Abstract
The characterized nuclear cyclic AMP responsive element (CRE)- and activator protein 1 (AP-1) DNA-binding activities in various brain regions of lethargic ( lh/lh) mice, a genetic model of absence seizures. Gel-shift assays showed that nuclear CRE- and AP-1 DNA-binding activities in the thalamus and cerebral cortex, but not in other regions such as the hippocampus and cerebellum of lethargic mice were significantly higher than those of non-epileptic control mice. Furthermore, CRE- and AP-1 DNA-binding activities in lethargic mice, but not control mice, were inhibited by the specific GABA B receptor antagonist CGP 46831, at a dose which suppressed seizure behavior and spike and wave discharges. These results suggest that enhanced nuclear CRE- and AP-1 DNA-binding activities in the thalamocortical region are related to generation and/or propagation of absence seizures in lethargic mice.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
