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Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene.

Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene. Research Abstract Details 

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  • Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene. Abstract Text:

    mikako sakuraiMikako Sakurai,masayuki sekiguchiMasayuki Sekiguchi,ko zushidaKo Zushida,kazuyuki yamadaKazuyuki Yamada,satoshi nagamineSatoshi Nagamine,tomohiro kabutaTomohiro Kabuta,keiji wadaKeiji Wada,mikako sakuraiMikako Sakurai,masayuki sekiguchiMasayuki Sekiguchi,ko zushidaKo Zushida,kazuyuki yamadaKazuyuki Yamada,satoshi nagamineSatoshi Nagamine,tomohiro kabutaTomohiro Kabuta,keiji wadaKeiji Wada,

    Overexpression of ubiquitin C-terminal hydrolase L1 (UCH-L1) in mice rescues amyloid beta-protein-induced decreases in synaptic plasticity and memory. However, the physiological role of UCH-L1 in the brain is not fully understood. In the present study, we investigated the role of UCH-L1 in the brain by utilizing gracile axonal dystrophy (gad) mice with a spontaneous deletion in the gene Uch-l1 as a loss-of-function model. Although gad mice exhibit motor paresis beginning at approximately 12 weeks of age, it is possible to analyse their brain phenotypes at a younger age when no motor paresis is evident. Maintenance of memory in a passive avoidance test and exploratory behaviour in an open field test were reduced in 6-week-old gad mice. The maintenance of theta-burst stimulation-induced long-term potentiation (LTP) of field synaptic responses from Schaffer collaterals to CA1 pyramidal cells in hippocampal slices was also impaired in gad mice. The LTP in gad mice was insensitive to actinomycin D, suggesting that a transcription-dependent component of the LTP is impaired. Phosphorylation of cyclic AMP response element binding protein (CREB) in the CA1 region of hippocampal slices from gad mice occurred earlier than in the slices from wild-type mice and was transient, suggesting that CREB phosphorylation is altered in gad mice. These results suggest that memory in passive avoidance learning, exploratory behaviour and hippocampal CA1 LTP are reduced in gad mice. We propose that UCH-L1-mediated maintenance of the temporal integrity and persistence of CREB phosphorylation underlies these impairments.

    Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene. Publishing Authors By Initials

    m sakuraiM Sakurai,m sekiguchiM Sekiguchi,k zushidaK Zushida,k yamadaK Yamada,s nagamineS Nagamine,t kabutaT Kabuta,k wadaK Wada,m sakuraiM Sakurai,m sekiguchiM Sekiguchi,k zushidaK Zushida,k yamadaK Yamada,s nagamineS Nagamine,t kabutaT Kabuta,k wadaK Wada,

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    Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: The European journal of neuroscience

    VOLUME: 27

    Page Numbers: 691-701

    Journal Abbreviation: Eur. J. Neurosci.

    ISSN: 1460-9568

    DAY: 18

    MONTH: Feb

    YEAR: 2008

    Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene. Information

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    LANGUAGE: eng

    NlmUniqueID: 8918110

    Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene. Keywords Mesh Terms:

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    Grant and Affiliation Information for Reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice with a spontaneous deletion in the ubiquitin C-terminal hydrolase L1 gene.

    AFFILIATION: Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan.

    Country: France

    France Research PublicationFrance Research Publication

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    MEDLINETA: Eur J Neurosci

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