Inducible knockout of the cyclin-dependent kinase 5 activator p35 alters hippocampal spatial coding and neuronal excitability

Eriko Kamiki, Roman Boehringer, Denis Polygalov, Toshio Ohshima*, Thomas J. McHugh

*この研究の対応する著者

研究成果: Article査読

3 被引用数 (Scopus)

抄録

p35 is an activating co-factor of Cyclin-dependent kinase 5 (Cdk5), a protein whose dysfunction has been implicated in a wide-range of neurological disorders including cognitive impairment and disease. Inducible deletion of the p35 gene in adult mice results in profound deficits in hippocampal-dependent spatial learning and synaptic physiology, however the impact of the loss of p35 function on hippocampal in vivo physiology and spatial coding remains unknown. Here, we recorded CA1 pyramidal cell activity in freely behaving p35 cKO and control mice and found that place cells in the mutant mice have elevated firing rates and impaired spatial coding, accompanied by changes in the temporal organization of spiking both during exploration and rest. These data shed light on the role of p35 in maintaining cellular and network excitability and provide a physiological correlate of the spatial learning deficits in these mice.

本文言語English
論文番号138
ジャーナルFrontiers in Cellular Neuroscience
12
DOI
出版ステータスPublished - 2018 5月 17

ASJC Scopus subject areas

  • 細胞および分子神経科学

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