The spatial and temporal representation of a tone on the guinea pig basilar membrane

Abstract

In the mammalian cochlea, the basilar membrane's (BM) mechanical responses are amplified, and frequency tuning is sharpened through active feedback from the electromotile outer hair cells (OHCs). To be effective, OHC feedback must be delivered to the correct region of the BM and introduced at the appropriate time in each cycle of BM displacement. To investigate when OHCs contribute to cochlear amplification, a laser-diode interferometer was used to measure tone-evoked BM displacements in the basal turn of the guinea pig cochlea. Measurements were made at multiple sites across the width of the BM, which are tuned to the same characteristic frequency (CF). In response to CF tones, the largest displacements occur in the OHC region and phase lead those measured beneath the outer pillar cells and adjacent to the spiral ligament by about 90°. Postmortem, responses beneath the OHCs are reduced by up to 65 dB, and all regions across the width of the BM move in unison. We suggest that OHCs amplify BM responses to CF tones when the BM is moving at maximum velocity. In regions of the BM where OHCs contribute to its motion, the responses are compressive and nonlinear. We measured the distribution of nonlinear compressive vibrations along the length of the BM in response to a single frequency tone and estimated that OHC amplification is restricted to a 1.25-to 1.40-mm length of BM centered on the CF place.cochlear amplifier ͉ outer hair cell ͉ frequency selectivity ͉ laser-diode interferometry v on Békésy (1) discovered that sound-induced stapes movement causes a wave of basilar membrane (BM) displacement to travel from the base of the cochlea to the apex because of a pressure difference set up across the cochlear partition. The length of the BM is graded in stiffness, and the cochlear partition can be modeled as a series of weakly coupled sections, each section comprised of a rigid mass connected to the sides of the cochlea by springs that decrease in stiffness toward the apex (2). The BM will resonate when the mechanical impedance caused by the stiffness of the springs cancels that caused by the mass of the section (1). At a point just basal to the resonant place, a peak of displacement will occur on the BM. At a point just apical to the resonant place, the BM impedance is insufficient to maintain a pressure difference across the cochlear partition, and the traveling wave dies out. The location of the displacement peak depends on stimulus frequency, so that each segment of the BM is tuned to a characteristic frequency (CF). von Békésy measured BM movement under postmortem conditions and found that the mechanical responses were broadly tuned and insensitive. Subsequent measurements made from sensitive cochleae in vivo have revealed that, in fact, BM displacement responses are sharply tuned and very sensitive at low sound-pressure levels (3-6).Contributions from the electromotile outer hair cells (OHCs) (7-10) appear to be essential for cochlear sensitivity and frequency tuning (11,12). Many current models of cochlear functi...

Reticular lamina and basilar membrane vibrations in living mouse cochleae

“…Data in Fig. 1 C and E demonstrate the high sensitivity, sharp tuning, and nonlinearity of basilar membrane responses to ultrasonic sounds in the living mouse cochlea, which are similar to previous measurements in squirrel monkeys (19), gerbils (20)(21)(22)(23), chinchillas (17,24,25), guinea pigs (26)(27)(28), and mice (7,29,30).…”

Finite-element model of the active organ of Corti

“…Then, the BM motion and the shearing motion between the TM and RL are calculated when the slice is driven either acoustically or electrically, and these results are also compared with previous experimental observations [5,[9][10][11]. The fully active response of the BM to acoustic excitation is then predicted, assuming small displacements, using a linear superposition of the calculated responses, with feedback provided by an appropriately defined gain function for the OHCs.…”

“…Non-invasive measurements of the internal motion within the organ of Corti are difficult, particularly in vivo in the fully active cochlea [4], but measurements with acoustic excitation of the partly active cochlea [5][6][7][8] are possible. Experimental observations of internal motion of the organ of Corti using in vivo or in vitro preparations have been reported, for acoustic excitation, by Nilsen & Russell [5], and Lee et al [9], by Nowotny & Gummer [9,10] for electrical excitation, by Chan & Hudspeth [11] for both excitation modes and by Fridberger et al [6] for static pressure loading. Even though there is still some debate about the role of the hair bundle dynamics [12 -18], it is widely believed that it is mainly the somatic motility of the OHCs that provides the power to drive the amplification of the vibration within the mammalian organ of Corti [3,19].…”

A morphogenetic wave ofp27Kip1transcription directs cell cycle exit during organ of Corti development

“…Although hair cells and supporting cells in the p27 Kip1 -null organ of Corti appear normal, and also appear to connect normally to neurons of the spiral ganglion, the animals are deaf, as assayed by a number of physiological parameters, including auditory brainstem responses and otoacoustic emissions (Chen and Segil, 1999;Lowenheim et al, 1999). While not ruling out the possibility that defects in other elements of the auditory system are responsible for the deafness of these mice, one possible explanation is that the delicate micromechanics of the organ of Corti (Nilsen and Russell, 2000) are disrupted by the presence of the supernumerary cells present in the mutant, and that the precise control of cell number by p27…”