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Ph.D. (1981)
University of Texas Health Science Center at Dallas

Hermes H. Yeh, Ph.D.
Professor of Pharmacology and Physiology in the Center for Aging and Developmental Biology

Primary Appointment:
Pharmacology and Physiology and Center for Aging and Developmental Biology

GEBS Cluster Affiliations:
CMM-Cellular and Molecular Basis of Medicine
NS-Interdepartmental Graduate Program in Neuroscience


Research:
Cellular and molecular mechanisms of neuroreceptor interactions and plasticity in the CNS

Training Program:
Multidisciplinary Training in Developmental Neuroscience (supported by the National Institute of Mental Health)


Contact Information:
E-mail: Hermes_Yeh@urmc.rochester.edu
Contact Information:
University of Rochester
School of Medicine and Dentistry
601 Elmwood Ave, Box 645
Rochester, New York 14642
Kornberg Medical Research Building, Room 1-9635
Phone: (585) 273-5688
Research Overview
Research in my laboratory revolves around issues related to the actions of neurotransmitters and the consequences of neurotransmitter receptor interactions on adult as well as developing neurons in the central nervous system. Within this context, my laboratory takes the view that neurons undergo constant adaptations in response to acute or chronic environmental changes and that this ultimately leads to altered patterns or efficiency of neurotransmission. Such plastic adaptations may occur in development, in response to neurodegenerative insults and may be manifest in alterations in neuronal morphology and/or functional properties, as well as in the molecular or genetic profiles of the neuron. Thus, my laboratory adopts a multidisciplinary approach, incorporating neuroanatomical, patch clamp electrophysiological and molecular biological techniques. My laboratory has also developed molecular biological techniques that can be combined with electrophysiology to analyze gene expression profiles and function in the same cell. The analysis at the level of single cells is now being extended to include the detection of proteins. This combined strategy is being employed in ongoing research projects to investigate GABA, glutamate and cholinergic receptors in development, including the influence of neurotrophins, and in an animal model of chronic alcoholism. These projects have in common the theme of revealing coordinated changes in function, the expression of genes and, ultimately, the encoded proteins.
Recent Publications

Sapp, D.W. and Yeh, H.H. (2000) Heterogeneity of GABAA receptor-mediated responses in the human IMR-32 neuroblastoma cell line. J. Neurosci. Res. 60: 504-510.

Signore, A.P and Yeh, H.H. (2000) Chronic exposure to ethanol alters GABAA receptor-mediated responses of layer II pyramidal cells in adult rat piriform cortex. J. Neurophysiol. 84: 247-254.

Lu, S-M., Zecevic, N., and Yeh, H.H. (2001) Distinct NMDA and AMPA receptor-mediated responses in mouse and human Cajal-Retzius cells. J. Neurophysiol. 86:2642-2646.

Yeh, H.H., Lu, S-M., and Therianos, S. (2002) Patch-clamp recording and expression profiling of candidate genes in single neurons. In: Methods in Alcohol Research (Liu, Y. and Lovinger, D., eds.), CRC Press, pp. 83-98.

Aguayo, L.G., Peoples, R.W., Yeh, H.H., and Yevenes, G.I. (2002) GABAA receptors as modulatory sites of ethanol action: direct or indirect actions? Curr. Top. Med. Chem. 2:869-885.

Cheng, Q. and Yeh, H.H. (2003) Brain-derived neurotrophic factor attenuates mouse cerebellar granule cell GABAA receptor-mediated responses via postsynaptic mechanisms. J. Physiol. 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. Physiol. 550:103-111.

Eriscon, M., Haythornthwaite, A.R., Yeh, P.W. and Yeh, H.H. (2003) Brain-derived neurotrophic factor mitigates chronic ethanol-induced attenuation of GABA responses in cultured cerebellar granule cells. J. Neurosci. Res. 73:722-730.

Van Zundert, B., Alvarez, F.J., Tapia, J.C., Yeh, H.H. and Aguayo, L.G. (2003) Developmental-dependent action of microtubule depolymerization on the function and structure of synaptic glycine receptor clusters in spinal neurons. J. Neurophysiol. (in press).


 

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GEBS Clusters:
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