Many congratulations to Dr. Jun Ding for his tremendous research work for the past years and a recent publication in Nature Neuroscience in Dec 2011.

Dr. Jun Ding obtained his B.S. degree in biology from East China Normal University in Shanghai, and his M.S. degree from Shanghai Institute of Physiology, Chinese Academy of Sciences.

He obtained his PhD degree in neuroscience at Northwestern University, where he joined Dr. James Surmeier’s Lab in the Interdepartmental Neuroscience program and his dissertation research centered on cholinergic modulation of synaptic transmission in the striatum and adaptation of striatal neurons in Parkinson’s disease.  After that, he joined the laboratory of Bernardo Sabatini at Harvard Medical School to pursue his postdoctoral training.  At Harvard Medical School, he continues to study synaptic connectivity and physiological function of cortico-thalamo-basal ganglia circuitry. He is also actively engaged in developing state-of-the-art superresolution 2-photon imaging techniques in brain slice preparations. In July of 2012, he will join Stanford Institute of Neuro-Innovation and Translational Neuroscience (SINTN) at Stanford University as an Assistant Professor in Department of Neuorology and Neurological Sciences.

In his Nature Neuroscience paper (Semaphorin 3E-Plexin-D1 signaling controls pathway-specific synapse formation in the striatum, 2011, Dec 18, doi:10.1038/nn.3003. [Epub ahead of print]), Dr Jun Ding and his colleagues determined the important role of Sema3E–Plexin-D1 signaling for the selective formation of thalamostriatal. Normal brain function requires specifically inter-connected neural networks. However, little is known about how specific synaptic connections are formed within the basal ganglia during development. In order to examine this fundamental question, they interrogated the formation of corticostriatal and thalamostriatal glutamatergic synapses, the two major glutamatergic inputs to the striatum. Using combination of electrophysiology, 2-photon laser scanning imaging and optogenetic tools, they demonstrated that Sema3E–Plexin-D1 signaling regulates spine density and synaptogenesis of striatal MSNs. They further identified that thalamostriatal inputs but not corticostriatal inputs are specifically regulated by Sema3E–PlexinD1 signaling. These findings reveal for the first time some of the molecular mechanisms that control the specific formation of glutamatergic inputs in the striatum. This work is published in recent issue of Nature Neuroscience.

If anyone is interested in more information, you are welcome to contact Dr. Jun Ding via Email: dingjun@stanford.edu
Cheers

HMS-CSSA