SINTN Stanford Institute for Neuro-Innovation & Translational Neurosciences

The Stanford Neurosciences Institute
proudly announces a research seminar by

Troy Littleton

"Calcium Regulation of Neurotransmitter Release, Synaptic Plasticity and Glial-Neuronal Signaling"

October 25th, 2012 - 4:30 - Clark Auditorium

Troy Littleton M.D./Ph.D.

Department of Biology
The Picower Institute for Learning & Memory

Website: Littleton lab Web Site

A conversation with Troy Littleton with the Stanford group Neuwrite West can be streamed or downloaded here: Littleton conversation


The computational power of the brain depends on synaptic connections that link together billions of neurons. With the long-term goal of understanding how synaptic signaling regulates neuronal communication and connectivity, and how its dysfunction contributes to neurological disease, we have used Drosophila as a model system to characterize the molecular mechanisms underlying neurotransmitter release and synaptic growth and plasticity. Recent findings from our lab and others have begun to identify the machinery that functions to sense calcium rises in nerve terminals during activity and trigger information transfer between neurons through vesicle fusion and the release of neurotransmitters. Presynaptically, calcium influx following an action potential initiates synaptic vesicle fusion and the release of neurotransmitters by activating the synaptic vesicle calcium sensor Synaptotagmin 1 and removing the SNARE binding fusion clamp provided by Complexin. Postsynaptically, calcium influx through neurotransmitter receptors or voltage-gated channels triggers synapse-specific plasticity. We have discovered that Synaptotagmin 4 is an evolutionarily conserved Synaptotagmin homolog that localizes to the postsynaptic compartment and mediates calcium-dependent postsynaptic vesicle fusion and the release of retrograde signals that trigger synaptic growth and plasticity. These data suggest Synaptotagmin 4 regulates activity-dependent release of postsynaptic retrograde signals that promote synaptic plasticity, similar to the role of Synaptotagmin 1 as a calcium sensor for presynaptic vesicle fusion. Recent genetic screens for epilepsy mutants in the lab has also uncovered a role for a calcium signaling pathway within glial cells that acutely regulates neuronal excitability. Glia exhibit large fluctuations in intracellular calcium both spontaneously and in response to neuronal activity, although the influence of glial calcium transients on neuronal signaling is not well understood. I will present our studies in Drosophila that examine the role of calcium signaling in neurotransmitter release, synaptic plasticity and acute glial-neuronal signaling.

Recent Papers:

Cho, R., Song, Y. & Littleton, J.T. (2010) Comparative analysis of Drosophila and mammalian complexins as fusion clamps and facilitators of neurotransmitter release. Mol. Cell. Neuroscience 45, 389-397.

[2] Yoshihara, M., Guan, Z. & Littleton J.T. (2010) Differential regulation of synchronous versus asynchronous neurotransmitter release by the C2 domains of Synaptotagmin 1. PNAS 107, 14869-14874.

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