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The Journal of Neuroscience, January 25, 2006, 26(4):1303-1313; doi:10.1523/JNEUROSCI.2699-05.2006

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Cellular/Molecular
Synaptic Vesicle Protein 2 Enhances Release Probability at Quiescent Synapses

Kenneth L. Custer,^1,3 Naola S. Austin,¹ Jane M. Sullivan,² and Sandra M. Bajjalieh¹

¹Departments of Pharmacology and ²Physiology and Biophysics and ³Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98103

Correspondence should be addressed to Sandra Bajjalieh, Box 357280, University of Washington, Seattle, WA 98103. Email: bajjalie{at}u.washington.edu

We report a thorough analysis of neurotransmission in cultured hippocampal neurons lacking synaptic vesicle protein 2 (SV2), a membrane glycoprotein present in all vesicles that undergo regulated secretion. We found that SV2 selectively enhances low-frequency neurotransmission by priming morphologically docked vesicles. Loss of SV2 reduced initial release probability during a train of action potentials but had no effect on steady-state responses. The amount and decay rate of asynchronous release, two measures sensitive to presynaptic calcium concentrations, are not altered in SV2 knock-outs, suggesting that SV2 does not act by modulating presynaptic calcium. Normal neurotransmission could be temporarily recovered by delivering an exhaustive stimulus train. Our results indicate that SV2 primes vesicles in quiescent neurons and that SV2 function can be bypassed by an activity-dependent priming mechanism. We propose that SV2 action modulates synaptic networks by ensuring that low-frequency neurotransmission is faithfully conveyed.

Key words: SV2; exocytosis; levetiracetam; synaptic transmission; synaptic vesicle release; neurosecretion; neurotransmission

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Received Jun. 30, 2005; revised Nov. 29, 2005; accepted Dec. 15, 2005.

Correspondence should be addressed to Sandra Bajjalieh, Box 357280, University of Washington, Seattle, WA 98103. Email: bajjalie{at}u.washington.edu

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