{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:08:12Z","timestamp":1790222892301,"version":"4.1.0"},"reference-count":69,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,6,27]],"date-time":"2016-06-27T00:00:00Z","timestamp":1466985600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK093953"],"award-info":[{"award-number":["R01DK093953"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30NS069271"],"award-info":[{"award-number":["P30NS069271"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Post\u2010tetanic potentiation (PTP) is attributed mainly to an increase in release probability (<jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub>) and\/or readily\u2010releasable pool (RRP) in many synapses, but the role of endocytosis in PTP is unknown.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Using the calyx of Held synapse from tissue\u2010specific dynamin\u20101 knockout (cKO) mice (P16\u201320), we report that cKO synapses show enhanced PTP compared to control.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We found significant increases in both spontaneous excitatory postsynaptic current (spEPSC) amplitude and RRP size (estimated by a train of 30 APs at 100\u00a0Hz) in cKO over control during PTP.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Actin depolymerization blocks the increase in spEPSC amplitude in both control and cKO, and it abolishes the enhancement of PTP in cKO. PTP is sensitive to the PKC inhibitor GF109203X in both control and cKO.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We conclude that an activity\u2010dependent quantal size increase contributes to the enhancement of PTP in cKO over control and an altered endocytosis affects short\u2010term plasticity through quantal size changes.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>High\u2010frequency stimulation leads to post\u2010tetanic potentiation (PTP) at many types of synapses. Previous studies suggest that PTP results primarily from a protein kinase C (PKC)\u2010dependent increase in release probability (<jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub>) and\/or readily\u2010releasable pool (RRP) of synaptic vesicles (SVs), but the role of SV endocytosis in PTP is unknown. Using the mature calyx of Held (P16\u201320), we report that tissue\u2010specific ablation of dynamin\u20101 (cKO), an endocytic protein crucial for SV regeneration, enhances PTP in cKO over control. To explore the mechanism of this enhancement, we estimated the changes in paired\u2010pulse ratios (PPRs) and RRP size during PTP. RRP was estimated by the back\u2010extrapolation of cumulative EPSC amplitudes during a train of 30 action potentials at 100\u00a0Hz (termed RRP<jats:sub>train<\/jats:sub>). We found an increase in RRP<jats:sub>train<\/jats:sub> during PTP in both control and cKO, but no significant changes in the PPR. Moreover, the amplitude and frequency of spontaneous excitatory postsynaptic currents (spEPSCs) increased during PTP in both control and cKO; however, the spEPSC amplitude in cKO during PTP was significantly larger than in control. Actin depolymerization reagent latrunculin\u2010B (Lat\u2010B) abolished the activity\u2010dependent increase in spEPSC amplitude in both control and cKO, but selectively blocked the enhancement of PTP in cKO, without affecting PTP in control. PKC inhibitor GF109203X nearly abolished PTP in both control and cKO. These data suggest that the quantal size increase contributes to the enhancement of PTP in dynamin\u20101 cKO, and this change depends on strong synaptic activity and actin polymerization.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp271937","type":"journal-article","created":{"date-parts":[[2016,5,27]],"date-time":"2016-05-27T09:18:50Z","timestamp":1464340730000},"page":"193-206","source":"Crossref","is-referenced-by-count":15,"title":["Dynamin\u20101 deletion enhances post\u2010tetanic potentiation and quantal size after tetanic stimulation at the calyx of Held"],"prefix":"10.1113","volume":"595","author":[{"given":"Satyajit","family":"Mahapatra","sequence":"first","affiliation":[{"name":"Department of Neuroscience School of Medicine and Public Health University of Wisconsin\u2010Madison  Madison WI 53706 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