Research in this laboratory, under the direction of Dr. Edward J. Walsh and in collaboration with Dr. JoAnn McGee, is directed toward understanding the normal development of vertebrate auditory systems, as well as the pathological basis of congenital and environmentally-induced deafness. Single neuron data acquired from both in vivo and in vitro brainstem preparations, as well as far- and near-field auditory evoked potentials and otoacoustic emissions, are used in conjunction with neuropharmacological procedures to investigate the development of sensory cell and neural coding within the auditory system.
Current research topics include:
- A study of the role of thyroid hormone as a necessary transcriptional factor in the development of sensory and neural processing (both afferent and efferent) in the auditory system.
- An experimental investigation of the functional role(s) of efferent (olivocochlear) projections onto sensory cells within the cochlea and neurotransmitter systems associated with those projections.
- Studies designed to consider the physiological consequences of naturally occurring mutations or targeted mutagenesis of a variety of genes that produce proteins that are necessary for normal auditory development or that produce progressive deafness.
- Studies designed to examine the developmental effects of chemically- or environmentally-induced toxicity on mechanical transduction within the cochlea and brainstem function (e.g., goitrogenic agents [propylthiouracil; methimazole], polychlorinated biphenyls [PCBs], organophosphates, and nicotine).
The laboratory is equipped to conduct neurophysiological (single neuron and ensemble evoked response), neuropharmacological and otoacoustic experiments. It includes a large, standard double-walled sound-attenuating room, two smaller booths, and microelectrode fabrication and histological facilities. Major electronic equipment includes devices for sound delivery, electrophysiological and acoustical recordings, microionophoresis and pressure-phoresis, and calibration. Pentium computers interfaced to 16-bit D/A and A/D converters and event timers control digital stimulus generation and real-time data acquisition and display utilizing custom-written software.
Sanes, D.H., McGee, J. & Walsh, E.J. (1998). Metabotropic glutamate receptor activation modulates sound level processing in the cochlear nucleus. J. Neurophysiol. 80, 209-217.
Walsh, E.J., McGee, J., McFadden, S.L. & Liberman, M.C. (1998). Long-term effects of sectioning the olivocochlear bundle in neonatal cats. J. Neurosci. 18, 3859-3869.
Cai, Y., McGee, J. & Walsh, E.J. (2000). Contributions of ion conductances to the onset responses of octopus cells in the ventral cochlear nucleus: Simulation results. J. Neurophysiol. 83, 301-314.
Snyder, R.L., Sinex, D.G., McGee, J. & Walsh, E.J. (2000). Acute spiral ganglion lesions change the tuning properties and tonotopic organization of cat inferior colliculus neurons. Hear. Res. 147, 200-220.
McGee, J. & Walsh, E.J. (2001). Mouse models for Usher and Alport Syndromes. In J. Willott (Ed.), Handbook of Mouse Auditory Research: From Behavior to Molecular Biology. CRC Press, Boca Raton, pp. 557-579.
Walsh, E.J. & McGee, J. (2001). Hypothyroidism in the Tshr mutant mouse. In J. Willott (Ed.), Handbook of Mouse Auditory Research: From Behavior to Molecular Biology. CRC Press, Boca Raton, pp. 537-555.