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

Overexpression of ubiquitin C‐terminal hydrolase L1 (UCH‐L1) in mice rescues amyloid β‐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...

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Veröffentlicht in:	The European journal of neuroscience 2008-02, Vol.27 (3), p.691-701
Hauptverfasser:	Sakurai, Mikako, Sekiguchi, Masayuki, Zushida, Ko, Yamada, Kazuyuki, Nagamine, Satoshi, Kabuta, Tomohiro, Wada, Keiji
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer's disease Animals Avoidance Learning - physiology Brain - enzymology Brain - physiopathology CREB Cyclic AMP Response Element-Binding Protein - metabolism Exploratory Behavior - physiology Fear - physiology Gene Deletion Gene Expression Regulation, Enzymologic - genetics hippocampus Hippocampus - enzymology Hippocampus - physiopathology Learning Disorders - genetics Learning Disorders - metabolism Learning Disorders - physiopathology Long-Term Potentiation - genetics LTP Male Memory Disorders - genetics Memory Disorders - metabolism Memory Disorders - physiopathology Mental Disorders - genetics Mental Disorders - metabolism Mental Disorders - physiopathology Mice Mice, Inbred C57BL Mice, Neurologic Mutants Mutation - genetics Neuronal Plasticity - genetics Phosphorylation transcription Ubiquitin - metabolism Ubiquitin Thiolesterase - genetics Wallerian Degeneration - genetics Wallerian Degeneration - metabolism Wallerian Degeneration - physiopathology
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