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Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice. / Li, Lian; Chin, Lih Shen; Shupliakov, Oleg; Brodin, Lennart; Sihra, Talvinder S.; Hvalby, Øivind; Jensen, Vidar; Zheng, Dake; Mcnamara, James O.; Greengard, Paul; Andersen, Per.

в: Proceedings of the National Academy of Sciences of the United States of America, Том 92, № 20, 26.09.1995, стр. 9235-9239.

Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование

Harvard

Li, L, Chin, LS, Shupliakov, O, Brodin, L, Sihra, TS, Hvalby, Ø, Jensen, V, Zheng, D, Mcnamara, JO, Greengard, P & Andersen, P 1995, 'Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice', Proceedings of the National Academy of Sciences of the United States of America, Том. 92, № 20, стр. 9235-9239. https://doi.org/10.1073/pnas.92.20.9235

APA

Li, L., Chin, L. S., Shupliakov, O., Brodin, L., Sihra, T. S., Hvalby, Ø., Jensen, V., Zheng, D., Mcnamara, J. O., Greengard, P., & Andersen, P. (1995). Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice. Proceedings of the National Academy of Sciences of the United States of America, 92(20), 9235-9239. https://doi.org/10.1073/pnas.92.20.9235

Vancouver

Li L, Chin LS, Shupliakov O, Brodin L, Sihra TS, Hvalby Ø и пр. Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice. Proceedings of the National Academy of Sciences of the United States of America. 1995 Сент. 26;92(20):9235-9239. https://doi.org/10.1073/pnas.92.20.9235

Author

Li, Lian ; Chin, Lih Shen ; Shupliakov, Oleg ; Brodin, Lennart ; Sihra, Talvinder S. ; Hvalby, Øivind ; Jensen, Vidar ; Zheng, Dake ; Mcnamara, James O. ; Greengard, Paul ; Andersen, Per. / Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice. в: Proceedings of the National Academy of Sciences of the United States of America. 1995 ; Том 92, № 20. стр. 9235-9239.

BibTeX

@article{1b6975f0a67849658f48e8bb92b5d5d8,
title = "Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice",
abstract = "Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organization of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area. This was in contrast to the organized vesicle clusters present in terminals of wild-type animals. Release of glutamate from nerve endings, induced by K+, 4-aminopyridine, or a Ca2+ ionophore, was markedly decreased in synapsin I mutant mice. The recovery of synaptic transmission after depletion of neurotransmitter by high-frequency stimulation was greatly delayed. Finally, synapsin I-deficient mice exhibited a strikingly increased response to electrical stimulation, as measured by electrographic and behavioral seizures. These results provide strong support for the hypothesis that synapsin I plays a key role in the regulation of nerve terminal function in mature synapses.",
author = "Lian Li and Chin, {Lih Shen} and Oleg Shupliakov and Lennart Brodin and Sihra, {Talvinder S.} and {\O}ivind Hvalby and Vidar Jensen and Dake Zheng and Mcnamara, {James O.} and Paul Greengard and Per Andersen",
year = "1995",
month = sep,
day = "26",
doi = "10.1073/pnas.92.20.9235",
language = "English",
volume = "92",
pages = "9235--9239",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "20",

}

RIS

TY - JOUR

T1 - Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice

AU - Li, Lian

AU - Chin, Lih Shen

AU - Shupliakov, Oleg

AU - Brodin, Lennart

AU - Sihra, Talvinder S.

AU - Hvalby, Øivind

AU - Jensen, Vidar

AU - Zheng, Dake

AU - Mcnamara, James O.

AU - Greengard, Paul

AU - Andersen, Per

PY - 1995/9/26

Y1 - 1995/9/26

N2 - Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organization of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area. This was in contrast to the organized vesicle clusters present in terminals of wild-type animals. Release of glutamate from nerve endings, induced by K+, 4-aminopyridine, or a Ca2+ ionophore, was markedly decreased in synapsin I mutant mice. The recovery of synaptic transmission after depletion of neurotransmitter by high-frequency stimulation was greatly delayed. Finally, synapsin I-deficient mice exhibited a strikingly increased response to electrical stimulation, as measured by electrographic and behavioral seizures. These results provide strong support for the hypothesis that synapsin I plays a key role in the regulation of nerve terminal function in mature synapses.

AB - Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organization of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area. This was in contrast to the organized vesicle clusters present in terminals of wild-type animals. Release of glutamate from nerve endings, induced by K+, 4-aminopyridine, or a Ca2+ ionophore, was markedly decreased in synapsin I mutant mice. The recovery of synaptic transmission after depletion of neurotransmitter by high-frequency stimulation was greatly delayed. Finally, synapsin I-deficient mice exhibited a strikingly increased response to electrical stimulation, as measured by electrographic and behavioral seizures. These results provide strong support for the hypothesis that synapsin I plays a key role in the regulation of nerve terminal function in mature synapses.

UR - http://www.scopus.com/inward/record.url?scp=0029059605&partnerID=8YFLogxK

U2 - 10.1073/pnas.92.20.9235

DO - 10.1073/pnas.92.20.9235

M3 - Article

C2 - 7568108

AN - SCOPUS:0029059605

VL - 92

SP - 9235

EP - 9239

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 20

ER -

ID: 40837008