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The Journal of Neuroscience, May 24, 2006, 26(21):5767-5776; doi:10.1523/JNEUROSCI.0289-06.2006

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Cellular/Molecular
Analysis of Knock-Out Mice to Determine the Role of HPC-1/Syntaxin 1A in Expressing Synaptic Plasticity

Tomonori Fujiwara,¹ Tatsuya Mishima,¹ Takefumi Kofuji,² Tomoki Chiba,^3,5 Keiji Tanaka,³ Akitsugu Yamamoto,⁴ and Kimio Akagawa¹

¹Department of Cell Physiology and ²Radio Isotope Laboratory, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan, ³Department of Molecular Oncology, Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo 113-8613, Japan, ⁴Department of Cell Biology, Nagahama Institute of Bio-Science and Technology, Nagahama, Shiga 526-0829, Japan, and ⁵Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaragi 305-8577, Japan

Correspondence should be addressed to Dr. Tomonori Fujiwara at the above address. Email: tfuj{at}kyorin-u.ac.jp

The protein HPC-1/syntaxin 1A is abundantly expressed in neurons and localized in the neuronal plasma membrane. It forms a complex with SNAP-25 (25 kDa synaptosomal-associated protein) and VAMP-2 (vesicle-associated membrane protein)/synaptobrevin called SNARE (a soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor) complex, which is considered essential for synaptic vesicle exocytosis; thus, HPC-1/syntaxin 1A is considered crucial for synaptic transmission. To examine the physiological function of HPC-1/syntaxin 1A in vivo, we produced knock-out (KO) mice by targeted gene disruption. Although HPC-1/syntaxin 1A expression was completely depleted without any effect on the expression of other SNARE proteins, the KO mice were viable. They grew normally, were fertile, and displayed no difference in appearance compared with control littermate. In cultured hippocampal neurons derived from the KO mice, the basic synaptic transmission in vitro was normal. However, the mutant mice had impaired long-term potentiation in the hippocampal slice. Also, although KO mice exhibited normal spatial memory in the hidden platform test, consolidation of conditioned fear memory was impaired. Interestingly, the KO mice had impaired conditioned fear memory extinction. These observations suggest that HPC-1/syntaxin 1A may be closely related to synaptic plasticity.

Key words: extinction; fear memory; HPC-1/syntaxin 1A; LTP; SNARE; synaptic plasticity

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Received Jan. 22, 2006; revised April 17, 2006; accepted April 17, 2006.

Correspondence should be addressed to Dr. Tomonori Fujiwara at the above address. Email: tfuj{at}kyorin-u.ac.jp

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