Exp Neurobiol 2011; 20(2): 92-99
Published online June 30, 2011
© The Korean Society for Brain and Neural Sciences
Bo-Ryoung Choi2, Kyoung Ja Kwon1, Seung Hwa Park3, Won Kyung Jeon4, Seol-Heui Han1, Hahn Young Kim1 and Jung-Soo Han2*
1Department of Neurology, Konkuk University Hospital, Center for Geriatric Neuroscience Research, IBST, Konkuk University, Seoul 143-729, 2Department of Biological Sciences & Center for Geriatric Neuroscience Research, IBST, Konkuk University, Seoul 143-701, 3Department of Anatomy, College of Medicine, Konkuk University, Seoul 143-729, 4Traditional Korean Medicine Converging Research Division, Korea Institute of Oriental Medicine, Daejeon 305-811, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-450-3293, FAX: 82-2-3436-5432
In the current investigation, the status of the septo-hippocampal cholinergic pathway and hippocampal mitogen-activated protein kinase (MAPK) signaling was examined in male Wistar rats with chronic cerebral hypoperfusion, which showed cognitive deficits based on assessment on a version of the Morris water maze. Chronic cerebral hypoperfusion was induced by bilateral common artery occlusion and maintained for 12 weeks until behavioral testing. Chronic cerebral hypoperfusion was shown to induce memory impairments and microglial activation in regions of white matter, including the fimbria of hippocampus. Choline acetyltransferase expression of the basal forebrain and expression of hippocampal MAPKs was decreased in rats with BCCAo compared to control rats. The results of this study suggest that cognitive decline induced by chronic cerebral hypoperfusion could be related to dysfunction of the basal forebrain cholinergic system and reduction of hippocampal MAPK activities.
Keywords: vascular dementia, neuroinflammation, memory, cholinergic, MAPK, hippocampus