The aim of the present study was to evaluate whether the activation of Cdk5, a protein that has been suggested to participate in higher cognitive functions, is required for the onset of a sensitized anxiety-related behavior induced by stress. The exposure to restraint enhanced both Cdk5 expression in certain subareas of the septohippocampal system, principally in the lateral septum (LS) and septal Cdk5 kinase activity in rats. Behaviorally, restrained wild type mice showed a behavior indicative of enhanced anxiety in the elevated plus maze (EPM). In contrast, unstressed mice and stressed knockout mice, which lacked the p35 protein, the natural activator of Cdk5, displayed similar anxiety-like behavior in the EPM. Finally, the intra-LS infusion of olomoucine - a Cdk5 inhibitor - blocked the enhanced anxiety in the EPM induced by prior stress in rats. All these data provide evidence that septal Cdk5 is required in the emergence of a sensitized emotional process induced by stress.
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http://dx.doi.org/10.1016/j.euroneuro.2008.02.007 | DOI Listing |
Mol Neurobiol
January 2016
Pathophysiology Department, Key Laboratory of Neurological Disease of Education Committee of China, China-Canada Cooperation Platform on Neurological Disorder, Institute of Brain Research, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Eur Neuropsychopharmacol
August 2008
Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba. Argentina.
The aim of the present study was to evaluate whether the activation of Cdk5, a protein that has been suggested to participate in higher cognitive functions, is required for the onset of a sensitized anxiety-related behavior induced by stress. The exposure to restraint enhanced both Cdk5 expression in certain subareas of the septohippocampal system, principally in the lateral septum (LS) and septal Cdk5 kinase activity in rats. Behaviorally, restrained wild type mice showed a behavior indicative of enhanced anxiety in the elevated plus maze (EPM).
View Article and Find Full Text PDFNeurochem Res
September 2008
Department of Physiology & Biophysics, University of Miami Miller School of Medicine, Miami, FL 33101, USA.
Activation of cyclin dependent kinases (Cdks) contributes to neuronal death following ischemia. We used oxygen-glucose deprivation (OGD) in septal neuronal cultures to test for possible roles of cell cycle proteins in neuronal survival. Increased cdc2-immunoreactive neurons were observed at 24 h after the end of 5 h OGD.
View Article and Find Full Text PDFNeuropharmacology
June 2003
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Hermann-Rein-Str. 3, 37075, Goettingen, Germany.
In this work, we confirm the novel role of cyclin-dependent kinase (Cdk) 5 in associative learning by demonstrating that injection of the Cdk5 inhibitor butyrolactone I into the lateral septum or hippocampus profoundly impaired context-dependent fear conditioning of C57BL/6J mice. However, unlike the inducible up-regulation of Cdk5 and its regulator p35 observed in Balb/c mice, high baseline levels, which were not affected by fear conditioning, were found in C57BL/6J mice. Surprisingly, microinjections of butyrolactone I into the lateral septum or hippocampus significantly decreased baseline Cdk5 activity within the entire septo-hippocampal circuitry, suggesting a functional link between septal and hippocampal Cdk5 activity.
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