Speaker: Eric Gruenstein, PhD
Professor Emeritus, Department of Molecular and Cellular Biosciences, University of Cincinnati Medical School
91福利 the speaker:聽 Eric Gruenstein is Professor Emeritus in the Department of Molecular & Cellular Biosciences at the University of Cincinnati College of Medicine. He received his undergraduate degree from Princeton University and his PhD in biochemistry from Duke University where he studied the mechanism of action of thyroid hormone. This was followed by a postdoctoral position in clinical endocrinology at the NIH and a second postdoc in cell biology at MIT where he studied non-muscle actin and was the first to show that it was different from muscle actin and that it changed its configuration when cells were transformed . In 1975 he joined the faculty at the University of Cincinnati Medical School as an assistant professor and he became a full professor in 1981. His lab鈥檚 early research included studies on Duchenne muscular dystrophy (DMD) and they were among the first to identify the protein product of the gene responsible for DMD. In 1992 he was awarded a Fogarty Senior International Fellowship for a sabbatical in the laboratory of Sir Michael Berridge at Cambridge University studying calcium signaling. An unanticipated result of that sabbatical was the founding of a new company called Intracellular Imaging Inc ( ) which by now has installed calcium imaging systems in numerous laboratories worldwide. Professor Gruenstein鈥檚 recent research has focused on calcium signaling in neurons and astrocytes.
At the personal level he has been married to his high school sweetheart for 61 years. They have three children and eight grandchildren. In 2024 they relocated from Cincinnati to Hampden, Maine to help their son and daughter-in-law, who are both physicians, raise their new granddaughter, Abby.
91福利 the seminar:
Background: In 1949 when Donald Hebb proposed a cellular mechanism underlying learning and memory (what has come to be called 鈥淣eurons that fire together wire together鈥� ), he had no idea of how that process might occur. In the intervening three quarters of a century since then, we have come to understand the way that process works in great detail at the cellular and molecular levels. The first thing we learned is that bursts of high frequency electrical activity by presynaptic neurons cause a long lasting increase in the strength of their synapses with their postsynaptic neurons. But this long term potentiation happens only if the postsynaptic neurons are successfully stimulated to fire their own action potentials. The mechanism for detecting the coordinated firing of pre- and post-synaptic activity relies on a specific type of neurotransmitter receptor called NMDA receptors, which require both the presynaptic release of glutamate and the depolarization of the postsynaptic membrane to become active. When this happens, the NMDA receptors open and Ca2+ flow into the postsynaptic neuron. The Ca2+ then activates a kinase enzyme, CaMK-II which has the unusual property of being able to phosphorylate itself. This autophosphorylatio allows it to become constitutively active and in this way it is able to create a prolonged increase in the strength of that synapse.
My Research: And so it was that I was intrigued when I first heard about a system of dissociated cortical neurons which, when cultured in vitro, organize themselves into a synaptically connected network that spontaneously starts to undergo synchronized Ca2+ oscillations. In my seminar I will describe studies in my lab aimed at elucidating the mechanism by which these Ca2+ oscillations are initiated and how they are synchronized. I will describe the effects that one of the causative factors in Alzheimer鈥檚 disease, apolipoprotein E, has on these neuronal calcium oscillations. I will also describe how dissociated neurons can be induced to form themselves into spherical clusters which then become connected by bundles of neurites and how they are affected by copper ions.
Please join us for this in person event in 107 Norman Smith Hall.





