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http://hdl.handle.net/1942/30306
Title: | Neurological characterization of mice deficient in GSK3α highlight pleiotropic physiological functions in cognition and pathological activity as Tau kinase | Authors: | Maurin, Hervé Lechat, Benoit DEWACHTER, Ilse Ris, Laurence Louis, Justin V Borghgraef, Peter Devijver, Herman Jaworski, Tomasz Van Leuven, Fred |
Issue Date: | 2013 | Publisher: | BMC | Source: | Molecular brain, 6 (1) (Art N° UNSP 27) | Abstract: | Background: GSK3β is involved in a wide range of physiological functions, and is presumed to act in the pathogenesis of neurological diseases, from bipolar disorder to Alzheimer’s disease (AD). In contrast, the GSK3α isozyme remained largely ignored with respect to both aspects. Results: We generated and characterized two mouse strains with neuron-specific or with total GSK3α deficiency.Behavioral and electrophysiological analysis demonstrated the physiological importance of neuronal GSK3α, with GSK3β not compensating for impaired cognition and reduced LTP. Interestingly, the passive inhibitory avoidance task proved to modulate the phosphorylation status of both GSK3 isozymes in wild-type mice, further implying both to function in cognition. Moreover, GSK3α contributed to the neuronal architecture of the hippocampal CA1 sub-region that is most vulnerable in AD. Consequently, practically all parameters and characteristics indicated that both GSK3 isoforms were regulated independently, but that they acted on the same physiological functions in learning and memory, in mobility and in behavior. Conclusions: GSK3α proved to be regulated independently from GSK3β, and to exert non-redundant physiological neurological functions in general behavior and in cognition. Moreover, GSK3α contributes to the pathological phosphorylation of protein Tau. | Keywords: | GSK3 alpha knock-out;Cognition;LTP;Protein Tau;Hippocampus;Motor behavior | Document URI: | http://hdl.handle.net/1942/30306 | e-ISSN: | 1756-6606 | DOI: | 10.1186/1756-6606-6-27 | ISI #: | 000319800000001 | Rights: | 2013 Maurin et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. | Category: | A1 | Type: | Journal Contribution |
Appears in Collections: | Research publications |
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1756-6606-6-27.pdf | Published version | 2.07 MB | Adobe PDF | View/Open |
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