Professor
and Chairman of the Department
Dr. Yeh graduated from DePauw University in 1976 and received the Ph.D. degree in Cell Biology with concentration in Neuroscience from the University of Texas Southwestern Medical Center at Dallas in 1981. He then trained at the National Institutes of Health as a Staff Fellow and joined the University of Rochester School of Medicine and Dentistry as an Assistant Professor of Neurobiology and Anatomy in 1984. He subsequently served on the faculty at Wake Forest University School of Medicine, where he was promoted to Professor of Physiology and Pharmacology, and the University of Connecticut Health Center, and returned to the University of Rochester in 2000 as part of the strategic plan to establish a Center for Aging and Developmental Biology. Dr. Yeh has taught actively in the medical school and graduate school curricula, and has had leadership roles in directing graduate education and training at the institutional and national levels.
Dr. Yeh’s research is neuroscience-oriented. The overriding theme targets the cellular and molecular mechanisms of neurotransmitter receptor interactions and their plasticity in the adult and developing CNS. His laboratory incorporates behavioral, neuroanatomical, patch clamp electrophysiological and molecular biological techniques to reveal and investigate coordinated adaptive changes in neuronal function, morphology, gene and protein expression. Such changes may become manifest as a result of acute or chronic insult during development, aging, in response to drugs of abuse or neurotoxicants. Ongoing research projects employ a variety of transgenic mouse models to investigate: (1) neurotrophins and the development of inhibitory and excitatory synaptic transmission; (2) neurotransmitters as developmental signals in the migration, specification and functional maturation of neurons; (3) cellular and molecular mechanisms in the septum and hippocampus that link enhanced spatial learning and memory with transgenically induced conditional gain of NGF function; (4) cellular and molecular mechanisms underlying the learning and memory deficits in chronic alcoholism. Graduate students and postdoctoral fellows are encouraged to elaborate on these research themes and cross-fertilize them with their own interests.
Cheng, Q. and Yeh, H.H. (2003) Brain-derived neurotrophic factor attenuates mouse cerebellar granule cell GABAA receptor-mediated responses via postsynaptic mechanisms. J. Physiology 548:711-721.
Chan, C-H. and Yeh, H.H. (2003) Enhanced GABAA receptor mediated activity following NMDA receptor activation in Cajal-Retzius cells in the developing mouse neocortex. J. Physiology 550:103-111.
Cheng, Q. and Yeh, H.H. (2004) PLCg signaling underlies BDNF potentiation of Purkinje cell responses to GABA. J. Neurosci. Res.79:616-627.
Wu, C-W. and Yeh, H.H. (2005) Nerve growth factor rapidly increases muscarinic tone in mouse medium septum/diagonal band of Broca. J. Neuroscience 25:4232-4242.
Cuzon, V., Yeh, P.W. and Yeh, H.H. (2005) Ambient GABA promotes cortical entry of tangentially migrating cells derived from the medial ganglionic eminence. Cerebral Cortex (Advance Access published December 7, 2005).Cheng, Q., P.W. Yeh, Yeh, H.H. (2006) Cajal-Retzius cells switch from expressing ?-less to ?-containing GABAA receptors during corticogenesis. Europ. J. Neurosci. 24:2145-2151.
Johnson, E.M., Craig, E. and Yeh, H.H. (2007) TrkB is necessary for pruning at the developing climbing fiber-Purkinje cell synapse. J. Physiology 582:629-646.
Cuzon, V., Yeh, P.W.L., Yanagawa, Y., Obata, K. and Yeh, H.H. (2008) Ethanol consumption during early pregnancy alters the disposition of tangentially migrating GABAergic interneurons in the fetal cortex. J. Neurosci. 28:1854-1864 (This Week in the Journal selection for the February 20th issue).
Hakjoo Lee, Stephen J. Raiker, Karthik Venkatesh, Rebecca Geary, Laurie A. Robak, Yu Zhang, Hermes H. Yeh, Peter Shrager, and Roman J. Giger (2008) Synaptic Function for the Nogo-66 Receptor NgR1: Regulation of Dendritic Spine Morphology and Activity-Dependent Synaptic Strength. J. Neurosci. 28: 2753-2765.
[8/14/08]