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The Journal of Neuroscience, January 11, 2006, 26(2):372-380; doi:10.1523/JNEUROSCI.3997-05.2006

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Cellular/Molecular
Synaptotagmin IV Does Not Alter Excitatory Fast Synaptic Transmission or Fusion Pore Kinetics in Mammalian CNS Neurons

Jonathan T. Ting,^1,2 Brooke G. Kelley,¹ and Jane M. Sullivan^1,2

¹Department of Physiology and Biophysics and ²Program in Neurobiology and Behavior, University of Washington School of Medicine, Seattle, Washington 98195

Synaptotagmin IV (Syt IV) is a brain-specific isoform of the synaptotagmin family, the levels of which are strongly elevated after seizure activity. The dominant hypothesis of Syt IV function states that Syt IV upregulation is a neuroprotective mechanism for reducing neurotransmitter release. To test this hypothesis in mammalian CNS synapses, Syt IV was overexpressed in cultured mouse hippocampal neurons, and acute effects on fast excitatory neurotransmission were assessed. We found neurotransmission unaltered with respect to basal release probability, Ca²⁺ dependence of release, short-term plasticity, and fusion pore kinetics. In contrast, expression of a mutant Syt I with diminished Ca²⁺ affinity (R233Q) reduced release probability and altered the Ca²⁺ dependence of release, thus demonstrating the sensitivity of the system to changes in neurotransmission resulting from changes to the Ca²⁺ sensor. Together, these data refute the dominant model that Syt IV functions as an inhibitor of neurotransmitter release in mammalian neurons.

Key words: fusion pore kinetics; kiss-and-run; short-term plasticity; calcium dependence; synaptic release probability; paired-pulse depression

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Received Sep 20, 2005; revised November 9, 2005; accepted November 10, 2005.

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