Event Abstract Back to Event Role of TRPM4 on cognitive function and hippocampal long term potentiation in chronic cerebral hypoperfused rats Nurul Aqmar Mohamad Nor Hazalin1, Liao Ping2 and Zurina Hassan1* 1 Universiti Sains Malaysia, Centre for Drug Research, Malaysia 2 National Neuroscience Institute, Calcium Signaling Laboratory, Singapore Chronic cerebral hypoperfusion (CCH) has been associated with the pathological process of neurodegeneration and cognitive impairment, which negatively impact the quality of life. Reduction in cerebral blood flow that arising in chronic cerebral hypoperfusion lead to selective neuronal injuries in vulnerable regions of the brain, especially hippocampus and subsequent cognitive impairment and motor dysfunction. Sustained activation of TRPM4 protein has been identified to play a critical role in cerebral vascular damage after ischaemic stroke. The present study aims to evaluate the functional impact of TRPM4 on cognitive function and electrophysiological measures of hippocampal integrity in CCH rats. The CCH rats were developed by permanently ligated common carotid arteries (PBOCCA) or sham-operated surgery. Immediately after operation, the rats were given 25-nmol siRNA intravenously. The results showed that TRPM4 inhibition by siRNA significantly improved spatial learning performance in the Morris water maze over a 5-day test period in PBOCCA rats. However, the inhibition did not affect the long term potentiation (LTP) recorded in the CA1 region of the hippocampus. It is feasible that other mechanisms may be compensated to support CA1 LTP. The findings warrant further investigation for TRPM4 to be a potential target for neuroprotective treatment strategy. Acknowledgements Financial support was received from Ministry of Higher Education (MOHE) Malaysia and Universiti Sains Malaysia special funding for the project of Fundamental Neuroscience-Neurobehaviour (304/CDADAH/652201/K134). Keywords: Cognition, Hippocampus, long term potentiation, in vivo, siRNA Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: O02: Postgraduate Travel Awardees Oral Session 2 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Mohamad Nor Hazalin N, Ping L and Hassan Z (2016). Role of TRPM4 on cognitive function and hippocampal long term potentiation in chronic cerebral hypoperfused rats. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00088 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Zurina Hassan, Universiti Sains Malaysia, Centre for Drug Research, Minden, Penang, 11800, Malaysia, Zurina.Hassan@frontiersin.org Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Nurul Aqmar Mohamad Nor Hazalin Liao Ping Zurina Hassan Google Nurul Aqmar Mohamad Nor Hazalin Liao Ping Zurina Hassan Google Scholar Nurul Aqmar Mohamad Nor Hazalin Liao Ping Zurina Hassan PubMed Nurul Aqmar Mohamad Nor Hazalin Liao Ping Zurina Hassan Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.