Synapsin-regulated synaptic transmission from readily releasable synaptic vesicles in excitatory hippocampal synapses in mice

  1. Øivind Hvalby1,
  2. Vidar Jensen1,
  3. Hung-Teh Kao2 and
  4. S. Ivar Walaas1
  1. 1Molecular Neurobiology Research Group, Institute of Basic Medical Sciences, University of Oslo, Norway2Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA
  1. Corresponding authorØ. Hvalby: Molecular Neurobiology Research Group, Institute of Basic Medical Sciences, University of Oslo, PO Box 1103 Blindern, 0317 Oslo, Norway. Email: o.c.hvalby{at}medisin.uio.no

Abstract

The effects of synapsin proteins on synaptic transmission from vesicles in the readily releasable vesicle pool have been examined by comparing excitatory synaptic transmission in hippocampal slices from mice devoid of synapsins I and II and from wild-type control animals. Application of stimulus trains at variable frequencies to the CA3-to-CA1 pyramidal cell synapse suggested that, in both genotypes, synaptic responses obtained within 2 s stimulation originated from readily releasable vesicles. Detailed analysis of the responses during this period indicated that stimulus trains at 2–20 Hz enhanced all early synaptic responses in the CA3-to-CA1 pyramidal cell synapse, but depressed all early responses in the medial perforant path-to-granule cell synapse. The synapsin-dependent part of these responses, i.e. the difference between the results obtained in the transgene and the wild-type preparations, showed that in the former synapse, the presence of synapsins I and II minimized the early responses at 2 Hz, but enhanced the early responses at 20 Hz, while in the latter synapse, the presence of synapsins I and II enhanced all responses at both stimulation frequencies. The results indicate that synapsins I and II are necessary for full expression of both enhancing and decreasing modulatory effects on synaptic transmission originating from the readily releasable vesicles in these excitatory synapses.

Footnotes

    • Accepted December 1, 2005.
    • Received October 27, 2005.
    • Revision received November 29, 2005.
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