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Laser interferometry was used to measure umbo velocity in the developing rat. The tympanic membrane was stimulated with pure tones between 0.4 and 40.0 kHz, at intensity levels between 50 and 130 dB SPL. The corresponding umbo velocity response was measured. Umbo velocity responded linearly with respect to sound pressure throughout development. When the stimulus level was held constant at 100 dB SPL, all animals displayed a velocity response that increased with frequency until a peak response was reached at about 20.0 kHz. Above this frequency the response decreased in all age groups. Umbo velocity increased with age at all frequencies, and at 1.0, 2.0, 4.0, 8.0, 16.0, and 32.0 kHz the velocity reached 90% of its mature value by 68, 24, 24, 15, 19, and 50 days after birth, respectively. These age-related increases in tympanic membrane velocity coincided with improvements in compound action potential (CAP) thresholds (as measured by other investigators) at similar frequencies. Both umbo velocity and CAP thresholds showed substantial growth after 10 days of age. The role of middle-ear functional development with respect to overall auditory sensitivity is discussed.

This presentation considers important developments and new trends related to acoustic injury in the peripheral auditory system reported during the past 5 years. The discussion begins with the effect overstimulation has on the "active" cochlear process, and the associated loss in receptive field (tuning curve) selectivity. Exposure to intense sound also changes the structure and function of the tectorial membrane, sensory hair bundles, tip links, and intracellular organelles. All of these injuries may change the way in which energy is delivered to the transduction channels of the hair cell. Important new evidence describing the quantitative relation between hair cell loss and permanent hearing loss is reviewed, and the possibility that specific exposure conditions cause unique lesions to the inner or outer hair cells is explored. Finally, the importance of hair cell regeneration in the chick cochlea, changes in the CNS following acoustic injury, and the cochlear vascular system are considered.

A high-frequency admittance meter was developed and used to study the maturation of physiological function in the middle ear of neonatal golden hamsters (Mesocricetus auratus). The middle-ear input admittance in the frequency range of 0.8-1.8 kHz was measured in animals ranging in age from 6 to 69 days postpartum. Admittance magnitude was found to increase steadily with age, beginning on day 16, to asymptotic values at each test frequency. There were no obvious differences in admittance growth rates within the range of frequencies tested. However, an analysis of the slopes of the admittance ma;nitude frequency response curves revealed an increase from 4.6 dB/octave for animals 25 days old or younger, to 6.3 dB/octave for all older animals. This difference between younger and older subjects indicates that the development of the middle ear in the golden hamster is more complex than a simple increase in pure compliance.

The design, calibration, and use of a noninvasive, noncontact device for stimulating hair cell hair bundles in vitro are described. This device employed a piezoelectric crystal, driven at high frequencies, to generate sinusoidal pressure in a contained fluid volume. The pressure was propagated to the tip of a glass micropipette and the oscillating water jet stimulus produced at the tip was used to stimulate sensory hair bundles. The movements of glass microbeads, caught in the oscillating pressure field of the water jet, provided a means of calibrating this stimulus. The linearity of the jet, its waveform and frequency response, the influence of pipette shape and tip diameter, as well as models to explain the operation of the water jet, are described. The use of this stimulus for measuring hair bundle micromechanics at high frequencies is then demonstrated.

Within the last 7 years, the protein actin has been identified in the stereocilia and cuticular plate region of the hair cell. An intensive effort has been mounted to describe the structural organization of this protein, to identify actin-associated proteins in these regions, and to identify the functional role of these proteins. The paracrystalline array of actin and its cross bridges imparts rigidity and stiffness to the stereocilia, which are important in determining their response properties. It also appears that these properties can be changed if the paracrystalline array is damaged by noise exposure. The functional implications of stereocilia rigidity and stiffness, as well as potential contractile mechanisms in the hair cell, are discussed. Finally, it is suggested that changes in the cross-sectional shape of the stereocilia caused by shearing of actin filaments during stereocilia deflections can be related to the mechano-electrical events in the plasma membrane of the cell. This may be the link between the transmission of vibrational energy through the sensory accessory structures of the peripheral ear, and the initiation of electrochemical events associated with transduction.

The anatomic consequences of acoustic overstimulation are explored in this presentation, and attention is directed toward issues where improvements in technology and empirical observation are needed before further advances in our understanding can be achieved. Gains have been made in the last decade in appreciating sound-induced cochlear injury, but there is now a need to evaluate not only cochlear pathology but also the functional state of the surviving structures. There is a wealth of information about the susceptibility of inner or outer hair cells to acoustic injury; however, the etiology of this injury is not yet fully understood. In addition, current ideas concerning the effects of noise on hair-cell stereocilia, hair-cell synapses, the cochlear vascular supply, and the central auditory pathways are in a state of flux and are either undergoing revision or emerging. Other issues, such as the basis of temporary or permanent threshold shift at the cellular level, and the individual differences in susceptibility to injury are in need of a fresh approach. It would seem that the time is now ripe to review our knowledge, recognize its gaps, and develop testable hypotheses concerning the mechanisms of acoustic injury to the ear.