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Electromotile hearing: Acoustic tones mask psychophysical response to high-frequency electrical stimulation of intact guinea pig cochlea)
a)Portions of this research were presented at the Midwinter Meetings of the Association for Research in Otolaryngology (for abstracts, see Le Prell et al., 2000 ; 2002 ).
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Image of FIG. 1.
FIG. 1.

Surgery-induced threshold shift was assessed as change in auditory brainstem response (ABR) threshold at 2, 4, 8 and . Data are shown for individual animals (CP83, CP91, P161, P163) to facilitate comparisons with psychophysical and morphological data. Threshold deficits were typically or less, although one animal (P163) had surgically induced threshold deficits of 20–, suggesting significant trauma during surgery. Consistent with this, we observed significant intra-cochlear bone growth in P163 at the time of euthanasia.

Image of FIG. 2.
FIG. 2.

Electrically evoked otoacoustic emissions (EEOAEs) were assessed in response to intra-cochlear electrical stimulation using a frequency sweep paradigm. Emissions were assessed using this paradigm for a single animal (P161); testing was conducted on day 45 postimplant. For all other subjects, testing was limited to 5.6, 8, 11.2, and , with each frequency presented at 0 (noise floor), 5, 10, 20, and as shown above using the frequency sweep paradigm. The results were equivalent in that EEOAE amplitude grew with increasing current level.

Image of FIG. 3.
FIG. 3.

Subjects were trained to report detection of 5.6 (A, B, C), 8 (D, E, F), 11.2 (G, H, I), and 16 (J, K, L) kHz acoustic signals. Once subjects were trained and producing reliable response latency functions, a process which typically required a total of 4–6 months, a ball electrode was implanted through the wall of the cochlea, into scala tympani, for delivery of sinusoidal electrical signals. Here, we illustrate detection response latency for 5.6, 8, 11.2, and acoustic test signals in quiet, with tests conducted over the first month postsurgery. Data are shown for subjects CP83 (A, D, G, J), CP91 (B, E, H, K) and P163 (C, F, I, J). Subjects were then switched to an electrical stimulus detection task. Subjects readily responded to electrical stimulation. Data shown here were collected during the first 1–2 months of testing; all data were collected in a quiet background. Responses were generally quite consistent, showing little improvement over any given 1–2 month test window, including the initial test period as illustrated here (response data are mean ). Threshold was defined as the sound level corresponding to a response latency of , see dashed lines.

Image of FIG. 4.
FIG. 4.

Subjects were retested in quiet in the detection task requiring response to 5.6, 8, 11.2, and sinusoidal signals delivered via intra-cochlear electrical stimulation of a ball electrode. Here, we illustrate detection response latency for test signals in quiet, with tests conducted at various times over 1–2 year periods. Pronounced improvement with long-term testing was observed for three subjects (CP83, CP91, P161), with thresholds improving up to re . All masking effects were therefore assessed relative to the most recent data in quiet.

Image of FIG. 5.
FIG. 5.

Subjects were trained to report detection of 5.6 (A, B, C, M), 8 (D, E, F, N), 11.2 (G, H, I, O), and 16 (J, K, L, P) kHz sinusoidal signals. Sinusoidal signals were acoustic during initial training, and later delivered using intra-cochlear electrical stimulation. Here, we illustrate the shift in electrical sinusoid detection thresholds when 10–dB SL acoustic pure-tone background maskers were presented (see axis). Target signal frequency is indicated in each panel using downwards arrows. Shift in detection threshold was calculated as the background-induced change from the most temporally proximate detection thresholds assessed in quiet; threshold shifts were greatest at frequencies closest to the electrical stimulation frequency except when the electrical target was a sinusoid. Anatomical evaluations were relatively normal in two animals (CP83, P161). The third animal (CP91) developed a sudden elevation in both acoustic and electrical signal detection thresholds and was found to have corresponding hair cell loss. In the fourth subject (P163, see right panels), the electrode was encased in bone.

Image of FIG. 6.
FIG. 6.

Whole-mount surface preparations of cochlear tissues from CP83 (left) and P161 (right). Actin filaments in the organ of Corti were labeled using rhodamine-phalloidin and visualized under epifluorescence. Tissues are from the basal turn (A, B), second turn (C, D), and third turn (E, F). Images were focused at the level of the OHC apical surface. Only mild and scattered OHC loss, consistent with age-related cell death (see Coleman 1976), was observed in these tissues (for examples, see arrows in panel A, where each arrow points at a site of a single missing OHC). IHC loss was generally not observed.

Image of FIG. 7.
FIG. 7.

Detection thresholds for electrical stimulation are plotted at all test frequencies (5.6, 8, 11.2, and ) for each of our subjects (CP83, CP91, P161, P163). In addition, we plot the lowest current level predicted to result in detectable electrical stimulation of auditory neurons in animals without outer hair cells (“Neural”). Electric detection thresholds for (bipolar) sinusoidal stimulation in a single deafened cat (taken from Smith et al., 1995) are consistent with the “predicted” neural thresholds. Empirically determined thresholds lower than the predicted neural stimulation thresholds are interpreted as the first direct perceptual evidence for the psychological phenomena termed “electromotile hearing”.


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752b84549af89a08dbdd7fdb8b9568b5 journal.articlezxybnytfddd
Scitation: Electromotile hearing: Acoustic tones mask psychophysical response to high-frequency electrical stimulation of intact guinea pig cochlea)