Melanie Woodin - 5th May - NEUReka! Seminar

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NEUReka Seminars

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Apr 25, 2016, 10:47:14 AM4/25/16
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Dear all,

We will be hosting Melanie Woodin for our next NEUReka! Seminar on 5th May at 1700 in the Gordon Museum.  Drinks and discussion to follow the seminar.  All are welcome!


Speaker - Melanie A. Woodin, Department of Cell and Systems Biology, University of Toronto

Title - "KCC2 Blurs the Lines between Excitatory and Inhibitory Synapses"

Time - 1700, Thursday 5th May

Venue - Gordon Museum, Hodgkin Building, Guy's Campus, King's College London

Host - Winnie Wefelmeyer (winnie.w...@kcl.ac.uk)


Abstract - 

Inhibitory synapses in the mature brain undergo activity-dependent synaptic plasticity.  The mechanism underlying this plasticity is a regulation of the K+-Cl- cotransporter (KCC2) required for maintaining low intracellular Cl-, which is essential for fast inhibitory transmission.  We recently discovered that KCC2 interacts with a kainate-type glutamate receptor subunit GluK2. This KCC2:GluK2 protein interaction is required for KCC2 oligomerization and protein expression.  While GluK2 is a subunit of an ionotropic receptor, kainate receptors can also signal metabotropically via a PKC-mediated signaling pathway. PKC is known to phosphorylate KCC2, which in turn increases its surface expression and function.  Thus we asked whether kainate receptor activation could regulate KCC2 function.  Specifically we hypothesized that activation of the kainate receptor metabotropic signaling pathway leads to an activation of PKC, which in turn phosphorylates KCC2 and increases its Cl- extrusion from the neuron.  We are testing this hypothesis using electrophysiology in hippocampal slices.  Specifically, we are recording the reversal potential for GABA (EGABA) as a measure of KCC2-mediated Cl- extrusion.  We found that stimulating metabotropic kainate receptor signaling leads to a significant hyperpolarization of EGABA.  Our results are revealing metabotropic kainate receptor signaling as a novel mechanism for regulating KCC2 function.    This talk will review these recent experiments examining kainate-receptor mediated metabotropic regulation of KCC2 function and discuss their physiological significance. Lastly I will highlight how these findings are increasingly blurring the lines between inhibition and excitation.



If you require any further information or directions to the venue please contact either Winnie Wefelmeyer (winnie.w...@kcl.ac.uk) or Chris Puhl (christop...@kcl.ac.uk).



We hope to see you there!


NEUReka! Organising Committee

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