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Signal transduction mechanisms involved in corticotropin releasing factor-mediated increase in neuronal excitability in the entorhinal cortex.

The entorhinal cortex (EC) is an essential component of the limbic system that is functionally found to be closely linked to emotional control, consolidation and recall of memories, Alzheimer's disease, schizophrenia and especially temporal lobe epilepsy. The EC serves as an interface to connect the hippocampus and other cortices. Corticotropin releasing factor (CRF), a neuropeptide, is known to be related to these physiological functions and neurological disorders. CRF is widely distributed in the brain including the limbic structures. Various studies suggest that the generation of epileptic seizures is related to the EC, hippocampus and amygdala. However, the signal transduction mechanisms involved in increase in the neuronal excitability leading to the epileptic seizures are not known. Here we studied the signaling mechanisms involved in CRF-mediated increase in neuronal excitability in the EC slices, using whole-cell recordings. Our results demonstrated that CRF increased the neuronal activity via activation of CRF2 receptors. We further demonstrated that G proteins, adenylate cyclase and protein kinase A were required for the increased neuronal excitability. With whole-cell patch-clamp recordings, we also showed that CRF increased action potential firing frequency by generating membrane depolarization.

Lalitha Kurada * and Saobo Lei.

Department of Physiology, Pharmacology and Therapeutics, University of North Dakota, Grand Forks, ND 58202.
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Title Annotation:Graduate Communications in the A. Roger Denison Competition
Author:Kurada, Lalitha; Lei, Saobo
Publication:Proceedings of the North Dakota Academy of Science
Article Type:Author abstract
Geographic Code:1USA
Date:Apr 1, 2012
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