[BIC-announce] FW: Dr Stefano Vicini- Killam Lecture Series - TODAY - Tuesday October 12th 4pm - GABAergic Control of Striatal Neurons

[Jennifer Chew, Ms.]

 FOR YOUR INFORMATION.  Jennifer 


Jennifer Chew
McConnell Brain Imaging Centre
MNI - WB317
3801 University Street
Montreal, Qc  H3A 2B4
Telephone:  514-398-8554
Fax:  514-398-2975



Killam Lecture

Speaker:  Stefano Vicini, PhD
Department of Physiology and Biophysics
Georgetown University School of Medicine Washington, DC

Title:  GABAergic Control of Striatal Neurons

Date:  TODAY

Place:  de Grandpre Communications Centre

Time:  4:00 pm
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Dr. Stefano Vicini
Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, DC

Title of talk: "GABAergic control of striatal neurons"

A delicate balance of information to and from the Striatum controls the execution of learned motor behaviors as well as the suppression of unwanted movements.  The main neuronal type in the Striatum, the medium spiny neuron (MSN), receives converging glutamatergic innervation from the Cortex and Thalamus and dopaminergic innervation from the Substantia Nigra. In addition a small population of GABAergic interneurons control the excitability of a vast population of MSNs to maintain the proper balance of information outflow for smooth control of motor output. This control is exerted via both excitatory synaptic action on AMPA and NMDA receptors and via phasic and tonic GABAa receptor activation. My two current funded projects aims to compare GABA and NMDA receptor-mediated currents and the receptor subtypes amongst MSNs originating the two antagonistic striatal outputs, the striatopallidal and the striatonigral pathways.  We are utilizing corticostriatal slices made from strains of mice which selectively express green or red  fluorescent protein in D1 or D2 dopamine receptor expressing cells to identify unique properties of GABAa receptors in these cells.

Striatopallidal and striatonigral neurons control movements and become imbalanced in movement disorders. Previous reports have suggested that dopamine depletion induces changes in GABA and NMDA receptors which exacerbate this imbalance of striatal output.  Using transgenic mice with the two major striatal output pathways labeled we are answering a fundamental question: What role tonic and phasic GABA and NMDA conductance plays in striatal disorders? We are studying the functional consequence of the activation of distinct dopamine receptors on NMDA and GABAa receptor subytpes. As these subtypes have a quite established pharmacology, our study has great potential to identify novel therapeutic targets for treating disorders associated with striatal dysfunction including Parkinson's disease, Huntington's disease, tardive dyskinesia, Tourette's syndrome and drug addiction. In addition, as the pharmacology of two major classes of DA receptors has such critical role in mental illness, the results we will derive, although clearly related to basic neuroscience, will have notable applications to both neurological disorders and to mental health.