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This Article Full Text Full Text (PDF) All Versions of this Article: 561/1/149    most recent jphysiol.2004.073494v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Samigullin, D. Articles by Bykhovskaia, M. Search for Related Content PubMed PubMed Citation Articles by Samigullin, D. Articles by Bykhovskaia, M.

¹ Lehigh University, Department of Biological Sciences, Bethlehem, PA, USA
² Institute of Biochemistry and Biophysics, Kazan, Russian Academy of Sciences, Russia

We investigated quantal release and ultrastructure in the neuromuscular junctions of synapsin II knockout (Syn II KO) mice. Synaptic responses were recorded focally from the diaphragm synapses during electrical stimulation of the phrenic nerve. We found that synapsin II affects transmitter release in a Ca²⁺-dependent manner. At reduced extracellular Ca²⁺ (0.5 mM), Syn II KO mice demonstrated a significant increase in evoked and spontaneous quantal release, while at the physiological Ca²⁺ concentration (2 mM), quantal release in Syn II KO synapses was unaffected. Protein kinase inhibitor H7 (100 µM) suppressed quantal release significantly stronger in Syn II KO synapses than in wild type (WT), indicating that Syn II KO synapses may compensate for the lack of synapsin II via a phosphorylation-dependent pathway. Electron microscopy analysis demonstrated that the lack of synapsin II results in an approximately 40% decrease in the density of synaptic vesicles in the reserve pool, while the number of vesicles docked to the presynaptic membrane remained unchanged. Synaptic depression in Syn II KO synapses was slightly increased, which is consistent with the depleted vesicle store in these synapses. At reduced Ca²⁺ frequency facilitation of synchronous release was significantly increased in Syn II KO, while facilitation of asynchronous release was unaffected. Thus, at the reduced Ca²⁺ concentration, synapsin II suppressed transmitter release and facilitation. These results demonstrate that synapsin II can regulate vesicle clustering, transmitter release, and facilitation.

(Received 6 August 2004; accepted after revision 21 September 2004; first published online 23 September 2004)
Corresponding author M. Bykhovskaia: Department of Biological Sciences, Lehigh University, Bethlehem, PA 18015, USA. Email: mabv{at}lehigh.edu

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