Loss of the synaptic vesicle protein SV2B results in reduced neurotransmission and altered synaptic vesicle protein expression in the retina

Catherine W. Morgans, Patricia Kensel-Hammes, James B. Hurley, Kimberly Burton, Rejean Idzerdal, G. Stanley McKnight, Sandra M. Bajjalieh

    Research output: Contribution to journalArticle

    32 Scopus citations

    Abstract

    The Synaptic Vesicle Protein 2 (SV2) family of transporter-like proteins is expressed exclusively in vesicles that undergo calcium-regulated exocytosis. Of the three isoforms expressed in mammals, SV2B is the most divergent. Here we report studies of SV2B location and function in the retina. Immunolabeling studies revealed that SV2B is detected in rod photoreceptor synaptic terminals where it is the primary isoform. In mice lacking SV2B, synaptic transmission at the synapse between photoreceptors and bipolar neurons was decreased, as evidenced by a significant reduction in the amplitude of the b-wave in electroretinogram recordings. Quantitative immunoblot analyses of whole eyes revealed that loss of SV2B was associated with reduced levels of synaptic vesicle proteins including synaptotagmin, VAMP, synaptophysin and the vesicular glutamate transporter V-GLUT1. Immunolabeling studies revealed that SV2B is detected in rod photoreceptor synaptic terminals where it is the primary isoform. Thus, SV2B contributes to the modulation of synaptic vesicle exocytosis and plays a significant role in regulating synaptic protein content.

    Original languageEnglish (US)
    Article numbere5230
    JournalPloS one
    Volume4
    Issue number4
    DOIs
    StatePublished - Apr 17 2009

    ASJC Scopus subject areas

    • Biochemistry, Genetics and Molecular Biology(all)
    • Agricultural and Biological Sciences(all)
    • General

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