Michael Greenberg (Harvard Medical School)
Molecular Biology Seminar Series
Carter Wallace Lecture
Michael E. Greenberg is the Chair of the Department of Neurobiology and Nathan Marsh Pusey Professor at Harvard Medical School. He received his Ph.D. from the Rockefeller University in 1982 and carried out his postdoctoral research at New York University Medical Center. After to joining the faculty at Harvard Medical School in 1986, Dr. Greenberg served as Director of the F.M. Kirby Neurobiology Center at Children’s Hospital Boston until his appointment as Chair of the Department of Neurobiology at Harvard Medical School in 2008.
Dr. Greenberg’s research has expanded our understanding of the molecular basis of the major events in neural development, the neural responses to injury and disease, and the potential for intervention, treatment, or cure. His research has also explored the molecular biology and genetics of autism spectrum disorders. More specifically, Dr. Greenberg and his research group focus on identifying mechanisms that trigger proliferation, differentiation and survival of neurons during development, and adaptive responses in the mature nervous system. Their work has uncovered the existence and function of a genetic program that is activated by neuronal activity, the mechanisms of signal transduction that carry the neuronal activity-dependent signal from the membrane to the nucleus, and the identification of regulators of this experience-dependent process that affect synapse development and plasticity. Dr. Greenberg is particularly interested in those activity-dependent processes whose dysfunction can lead to the development of diseases of cognitive function.
Dr. Greenberg is the recipient of a number of honors and awards for his research including the Edward M. Scolnick Prize in Neuroscience, the J. Allyn Taylor International Prize in Medicine, the Perl-UNC Neuroscience Prize, and the Julius Axelrod Award for the Society of Neuroscience. He holds membership in both the American Academy of Arts and Sciences and the National Academy of Science.
Signaling Networks that Regulate Synapse Development and Cognitive Function
Our interactions with the outside world trigger changes at neuronal synapses that are critical for proper brain development and higher cognitive function. Research in the Greenberg laboratory has focused on the identification of a genetic program that is activated by neuronal activity, the mechanisms of signal transduction that carry the neuronal activity-dependent signal from the membrane to the nucleus, and the identification of regulators of this experience-dependent process that affect synapse development and plasticity. Our recent studies using global screening techniques haveidentified a number of activity-dependent genes that control various processes such as 1) the complexity of the dendritic arbor, 2) the formation, maturation, and maintenance of spines, the post-synaptic sites of excitatory synapses, 3) the composition of protein complexes at the pre- and post-synaptic sites, 4) the relative number of excitatory and inhibitory synapses, and 5) the production and secretion of neuropeptides that control synaptic inhibition. These activity-regulated processes are critical for normal brain development and function, and defects in the activity-dependent gene program contribute to disorders of human cognition such as Rett Syndrome (RTT) and Angelman Syndrome (AS), two neurological disorders associated with syndromic autism. Understanding how the neuronal activity-dependent gene program functions may provide insight into how the dysregulation of this process leads to neurological diseases and, ultimately, may suggest therapies for treatment of disorders of cognitive function.
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