The study of the auditory function of the cochlea has progressed enormously over the last century. Nevertheless, the cochlea’s difficult accessibility to experimentation, its small size and its extreme mechanical delicacy have hampered the understanding of hearing physiology in comparison to other organs systems. There are many important questions that remain to be answered. Two central questions of cochlear physiology are: How does loud sound cause hearing loss? How do the sensory cells of the organ of Corti amplify and discriminate complex sounds?

To answer the first question, there are many research directions as sound can affect many cellular components of the inner ear. The Nuttall laboratory has been directing its efforts toward an understanding of the regulation of blood circulation to the cochlea as one important aspect of sound-induced hearing loss. The energy need of the cochlea is very high and it is important to maintain the appropriate blood circulation by vasodilative mechanisms. Nitric oxide (NO) is one molecular mechanism of vasodilation and NO at high concentration can also be toxic to cells. The laboratory is addressing both the cellular vasodilation mechanisms of cochlear-vascular smooth muscle and the multiple roles of NO in cochlear physiology/pathophysiology.

The second question has to do with the physiology of outer hair cells (OHCs). These cells have been discovered by other researchers to possess a kind of motility. The movement of the OHCs in response to electric or acoustic stimulation may amplify the movement of the sensory tissue as a whole. The physiological process that accomplishes the amplification is called the cochlear amplifier (CA) and its operation is not understood. The laboratory is studying the role of OHCs in the function of the CA by measuring the mechanical motion of inner ear tissues. Two fundamentally different approaches to the problem are used. In the first case measurements are being made of the micromechanical motion of the tissue. The desire is to measure the actual OHC motion in vivo and deep within the inner ear tissue rather than the superficial motion of the surface of the tissue. The second approach is to mathematically model the motion for clues on whether OHCs might generate mechanical power in the amplification process.

All of the studies of the laboratory have bearing on issues of hearing function and hearing loss. Blood flow is obviously of critical importance to the health of the cochlea, whereas the OHCs are the most vulnerable inner-ear cellular elements to all forms of damage (sound, age and toxic drugs).

Jiang, Z.G., Qiu, J., Ren, T., and Nuttall, A.L. Membrane properties and the excitatory junction potentials in smooth muscle cells of cochlea spiral modiolar artery in guinea pigs. Hear. Res. 138:171-180, 1999.

Nuttall, A.L. Sound-Induced Cochlear Ischemia/Hypoxia as a Mechanism of Hearing Loss: A Review, Laryngology and Otology, Noise and Health J, 5.17-31, 1999.

Parthasarathi, A.A., Grosh, K., and Nuttall, A.L. Three-dimensional numerical modeling for global cochlear dynamics J Acoust. Soc. Am. Jan; 107(1):474-85, 2000.

Ren, T., Nuttall, A.L. Fine Structure and Multicomponents of the Electrically Evoked Otoacoustic Emission in Gerbil. Hear. Res., 143:58-68, 2000.

de Boer, E. and Nuttall, A.L. The mechanical waveform of the basilar membrane. II. From data to models—and back. J. Acoust. Soc. Am. 107(3):1487-96, 2000.

Ren, T., Nuttall, A.L. and Parthasarathi, A.A, Quantitative measure of multicomponents of otoacoustic emissions. J. Neurosci. Met. 96:97-104, 2000.

Ren, T. and Nuttall, A.L. Basilar Membrane Vibration in the Basal Turns of the Sensitive Gerbil Cochlea. Hear. Res. 151:48-60, 2001.

Nuttall, A.L., Zheng, J., Ren, T., and de Boer, E. Electrically Evoked otoacoustic emissions from apical and basal perilymphatic electrode positions in the guinea pig cochlea. Hear. Res. 152 (1-2) 77-89, 2001.

Shi, X. and Nuttall, A.L. Nitric oxide distribution and production in the guinea pig cochlea. Hear. Res. 153 (1-2) 23-31, 2001.

Vass, Z., Steyger, P., Hordichok, A., Trune, D. Jancso, G., and Nuttall, A. L. Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability and cochlear and vertebro-basilar arteries: A potential cause of inner ear dysfunction in headache. J. Neurosci. 103(1)189-201, 2001.

Nuttall, A.L., Ren, T., de Boer, E., Zheng, J., Parthasarathi, A., Grosh, K., Guo, M., and Dolan, D. In vivo micromechanical measurements of the organ of Corti in the basal cochlear turn. Audiol. Neurootol. 7(1):21-26, 2002.

Shi, X., Ren, T., and Nuttall, A.L. The Electrochemical and fluorescence detection of nitric oxide in the cochlea. Hear. Res. 164:49-58, 2002.

Friderberger, A., Zheng, J. and Nuttall, A.L. Alterations of basilar membrane response phase and velocity following acoustic overstimulation. Hear. Res. 167:214-222, 2002.