Raymond J Dingledine (born December 17, 1948) is an American pharmacologist and neurobiologist who has made considerable contributions to the field of epilepsy. He serves as Professor in the School of Medicine at Emory University, Atlanta GA, where he chaired the pharmacology department for 25 years and served as Executive Associate Dean of Research for 10 years.[1]
Dingledine joined the Department of Pharmacology at the University of North Carolina Chapel Hill in 1978 as an Assistant Professor, rising to full Professor by 1989. Shortly after a sabbatical year at the Salk Institute in Steve Heinemann’s lab, he joined Emory University in 1992 as Chair of the Department of Pharmacology, a job he held until 2017. He also served as Executive Associate Dean of Research in the School of Medicine from 2004-2005 and 2008–2015.[1]
He has served in professional science-intensive organizations throughout his career. He served on the Program Advisory Committee of the Morehouse School of Medicine Neuroscience Institute from its inception in 1997 through 2021, chairing this committee for 14 years. He served the Society for Neuroscience in numerous functions including Treasurer in 2003 and, most recently, as Chair of their Investment Committee for 15 years. At the American Epilepsy Society he chaired the Epilepsy Benchmark Stewards from 2017-2018. From 1995 to 2000, he served as editor-in-chief of Molecular Pharmacology, a major journal sponsored by the American Society for Pharmacology and Experimental Therapeutics. Dingledine co-founded two small pharma companies. NeurOp Inc was founded in 2003 and is currently a clinical-stage company focused on developing NMDA receptor modulators for cerebral ischemia, pain and depression. He serves on NeurOp’s Board of Directors and Scientific Advisory Board.[3] Pyrefin Inc was founded in 2019 to develop novel anti-inflammatory drugs to combat cognitive decline and post-operative pain; he chairs Pyrefin’s Board of Directors.[4] He is an inventor of record for 10 awarded US patents.
Research and work
His early research focused on the modulation of glutamate receptor-mediated synaptic transmission.[5] During this period he and his team discovered that glycine is a coagonist rather than modulator of NMDA receptors,[6] that shrinkage of extracellular space mediates the transition between interictal and ictal states in the high potassium model of seizures,[7][8] that a single amino acid residue controls calcium permeation in glutamate receptor channels,[9] and that ifenprodil analogs inhibit NMDA receptors by increasing the sensitivity of receptors to proton inhibition.[10] His current research focuses on the myriad roles of neuroinflammation in neurologic disorders.[11] He demonstrated a profound role for EP2 receptor activation by prostaglandin E2 in COX-2 related pathologies.[12] His work highlights the importance of neuroinflammation in epilepsy.
^Traynelis, S. F.; Dingledine, R. (1 May 1989). "Role of extracellular space in hyperosmotic suppression of potassium-induced electrographic seizures". Journal of Neurophysiology. 61 (5): 927–938. doi:10.1152/jn.1989.61.5.927. PMID2723735.
^Traynelis, S. F.; Dingledine, R. (1 January 1988). "Potassium-induced spontaneous electrographic seizures in the rat hippocampal slice". Journal of Neurophysiology. 59 (1): 259–276. doi:10.1152/jn.1988.59.1.259. PMID3343603.
