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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.</jats:p>","journal":"Proceedings of the National Academy of Sciences","year":1995,"id":658197,"datarank":11.825178406577127,"base_score":5.834810737062605,"endowment":5.834810737062605,"self_citation_contribution":0.8752216105593909,"citation_network_contribution":10.949956796017736,"self_endowment_contribution":0.8752216105593909,"citer_contribution":10.949956796017736,"corpus_percentile":null,"corpus_rank":null,"citation_count":341,"citer_count":200,"citers_with_citation_signal":200,"citers_with_endowment":200,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":823942,"name":"L S Chin","orcid":null,"position":1,"is_corresponding":false},{"id":1718188,"name":"O Shupliakov","orcid":null,"position":2,"is_corresponding":false},{"id":1718189,"name":"L Brodin","orcid":null,"position":3,"is_corresponding":false},{"id":1718190,"name":"T S Sihra","orcid":null,"position":4,"is_corresponding":false},{"id":1718191,"name":"O Hvalby","orcid":null,"position":5,"is_corresponding":false},{"id":1718192,"name":"V Jensen","orcid":null,"position":6,"is_corresponding":false},{"id":1718193,"name":"D Zheng","orcid":null,"position":7,"is_corresponding":false},{"id":1718194,"name":"J O McNamara","orcid":null,"position":8,"is_corresponding":false},{"id":1528465,"name":"P Greengard","orcid":null,"position":9,"is_corresponding":false},{"id":534065,"name":"L Li","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice.","abstract":"<jats:p>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. 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