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231225s2017 xx |||||o 00| ||eng c |
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|a 10.1155/2017/4526417
|2 doi
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|a pubmed24n0932.xml
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|a (NLM)29318050
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Yang, Hua
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Brain-Specific SNAP-25 Deletion Leads to Elevated Extracellular Glutamate Level and Schizophrenia-Like Behavior in Mice
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|c 2017
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 30.07.2018
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|a Date Revised 18.02.2021
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Several studies have associated reduced expression of synaptosomal-associated protein of 25 kDa (SNAP-25) with schizophrenia, yet little is known about its role in the illness. In this paper, a forebrain glutamatergic neuron-specific SNAP-25 knockout mouse model was constructed and studied to explore the possible pathogenetic role of SNAP-25 in schizophrenia. We showed that SNAP-25 conditional knockout (cKO) mice exhibited typical schizophrenia-like phenotype. A significantly elevated extracellular glutamate level was detected in the cerebral cortex of the mouse model. Compared with Ctrls, SNAP-25 was dramatically reduced by about 60% both in cytoplasm and in membrane fractions of cerebral cortex of cKOs, while the other two core members of SNARE complex: Syntaxin-1 (increased ~80%) and Vamp2 (increased ~96%) were significantly increased in cell membrane part. Riluzole, a glutamate release inhibitor, significantly attenuated the locomotor hyperactivity deficits in cKO mice. Our findings provide in vivo functional evidence showing a critical role of SNAP-25 dysfunction on synaptic transmission, which contributes to the developmental of schizophrenia. It is suggested that a SNAP-25 cKO mouse, a valuable model for schizophrenia, could address questions regarding presynaptic alterations that contribute to the etiopathophysiology of SZ and help to consummate the pre- and postsynaptic glutamatergic pathogenesis of the illness
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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7 |
|a Snap25 protein, mouse
|2 NLM
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| 650 |
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7 |
|a Synaptosomal-Associated Protein 25
|2 NLM
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| 650 |
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7 |
|a Syntaxin 1
|2 NLM
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| 650 |
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7 |
|a Vesicle-Associated Membrane Protein 2
|2 NLM
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| 650 |
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7 |
|a vesicle-associated membrane protein 2, mouse
|2 NLM
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| 650 |
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7 |
|a Glutamic Acid
|2 NLM
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| 650 |
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7 |
|a 3KX376GY7L
|2 NLM
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| 700 |
1 |
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|a Zhang, Mengjie
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Shi, Jiahao
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhou, Yunhe
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wan, Zhipeng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Yicheng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wan, Yinghan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Jun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Zhugang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Fei, Jian
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Neural plasticity
|d 1998
|g 2017(2017) vom: 26., Seite 4526417
|w (DE-627)NLM098558390
|x 1687-5443
|7 nnns
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| 773 |
1 |
8 |
|g volume:2017
|g year:2017
|g day:26
|g pages:4526417
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| 856 |
4 |
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|u http://dx.doi.org/10.1155/2017/4526417
|3 Volltext
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|d 2017
|j 2017
|b 26
|h 4526417
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