Joshua Kaplan is a Professor at the Department of Neurobiology, Harvard Medical School (since 2010) and a Molecular Biologist at the Department of Molecular Biology, Massachusetts General Hospital. He received his B.S. in Biochemistry in 1982 from Yale University and went on to do a Ph.D. in Genetics with Dr. J. Michael Bishop and Harold Varmusin at the University of California, San Francisco. He carried out his postdoctoral research with Dr. H. Robert Horvitz, Massachusetts Institute of Technology, Cambridge, MA. He then accepted the positions as an Assistant Professor at department of Genetics, Harvard Medical School and at the Department of Molecular and Cell Biology, Division of Cell and Developmental Biology, University of California, at Berkeley.
From 1999 – 2002 he was an Associate Professor in the Department of Molecular and Cell Biology, Division of Cell and Developmental Biology, University of California, at Berkeley. Since 2002 he is back at Harvard Medical School as a Professor. He has been received numerous awards and Honours including the Javits Neuroscience Investigator Award of the National Institute of Neurological Disorders and Stroke (NINDS) in 2008. He has already visited Göttingen on previous occasions as a member of the scientific advisory board of the GGNB (Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences).
The central theme of Prof. Kaplan’s work is to utilize behavioral, genetic, biochemical, imaging, and electrophysiological techniques to study signaling in the brain of the worm C. elegans. Current work is focused on three areas: regulation of synaptic vesicle exo- and endocytosis, synaptic remodeling and plasticity, and metabolic control of synaptic transmission.
Synaptic plasticity and synaptic refinement in C. elegans
A hallmark of all nervous systems is that signaling within circuits is dynamically adjusted both during development and in response to experience. These modifications of neuronal circuits (which are generically termed synaptic plasticity) can occur both at the level of addition and removal of synaptic connections, and by regulation of pre-existing synapses. Synaptic plasticity is thought to play a pivotal role in learning, cognitive development, and its disruption may account for the neuronal defects in psychiatric disorders. Although C. elegans has been extensively utilized to identify genes required for synaptic transmission, much less is known about the genetic pathways governing synaptic plasticity in C. elegans. In the past few years, we have studied several forms of activity-dependent plasticity, all occurring at synapses between motor neurons and body wall muscles (termed neuromuscular junctions, or NMJs). These include: 1) a retrograde synaptic signal from muscles that inhibits acetylcholine (ACh) release from motor neurons; 2) a neuropeptide that stimulates ACh release; 3) Wnt regulated trafficking of nicotinic receptors; and 4) activity dependent remodeling of GABAergic NMJs. In his talk, he will describe their efforts to define the cell biological mechanisms involved in these forms of plasticity. In particular, he will focus on molecules that dictate the kinetics of neurotransmitter release, and how this could play an important role in shaping circuit development and function.
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