Inferior collicular lesions: effects on audiogenic seizure and Preyer reflex.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K R Henry.
Explore the source record for details and available documents.
We present examples of results from our studies of auditory primary afferent nerve fibers and populations of such fibers in the frog and gerbil. We take advantage of the natural dithering effect of internal noise, where it is sufficient, to construct highly predictive descriptive models (based on the Wiener series with kernels derived from white-noise analysis). Where the internal noise is insufficient, we enhance dithering by applying external acoustic noise together with our stimuli. Using acoustic noise as a background sound, orthogonal to the stimulus waveform, we show that under some circumstances such background sound can enhance the ability of individual fibers and populations of fibers to encode the stimulus waveform.
Volume-conducted auditory evoked potentials were simultaneously measured from the level of the ear to the inferior colliculus of mice. The C57BL/6 mouse, which displays genetic sensorineural progressive hearing loss, was compared with the CBA/J mouse. At 50 days post partum, amplitudes of the summating potential (SP) and cochlear microphonic (CM) were lower in the C57BL/6 genotype, and they decreased progressively with age. Fifty days later, changes were seen in responses from the auditory nerve and cochlear nucleus of this mouse. By 200 days of age, the C57BL/6 had a "recruitment" pattern at CNS regions, but not at the auditory nerve.
Remote (vertex-positive, volume-conducted) and local (round window, or RW) responses were simultaneously recorded from the C57BL/6 mouse. Volume-conducted responses were obtained which corresponded to the cochlear microphonic (CM), summating potential (SP), and action potential (AP), as measured at the RW. The vertex PI, corresponding to the AP, had a shorter latency to rarefaction than to condensation clicks. At higher SPL's bimodal PI peaks (a and b) were observed. PIb amplitudes were greater at lower, and PIa amplitudes were greater at higher SPL'S. Responses subsequent to the RW N1 and the volume-conducted P1 were eliminated after the ear was isolated from the brainstem.
C57BL/6 and CBA/J inbred strains of mice, from 20 to 385 days of age, were exposed to 65 dB acoustic clicks at rates of 10, 20, 40 and 80 per second. For both genotypes, increasing the stimulus repetition rate increased latencies by 66, 141, 163, 188, and 356 mu sec for PI-V of the BSER, respectively. For the CBA/J mouse, there was a concurrent decline of all BSER amplitudes by approximately 45%. The C57BL/6 mouse showed this same 45% decline for PI, PII and PIV, although its PIII and PV amplitudes only declined by 25% as the repetition rate increased. Age had no observable influence on these variables. When binaural and monaural responses were compared, all ages and genotypes showed the same effect. For PI-III, binaural stimulation produced the same effect as did summing the responses obtained by monaurally stimulating the two ears. For PIV and PV, however, binaural stimulation reduced the amplitudes by 25 and 71%, respectively. These results were compared with data obtained from the cat and human. Although the rate-dependent BSER changes varied as a function of genotype, no genetic differences were observed in the binaural interactive effect, in spite of large differences of hearing ability in these inbred strains of mice.
Surgical ligation of the external auditory canal of the Mongolian gerbil produces aural cholesteatomas that are similar to the spontaneous gerbilline cholesteatoma. Some 6-9 months after ligation of the external auditory canal, these cholesteatomas are in contact with the bone of the middle ear. These induced cholesteatomas were seen to erode bone and displace soft tissue structures, as is typical of human aural cholesteatomas. The induced gerbilline cholesteatoma is an ideal experimental model for the study of the osteolytic characteristics of cholesteatoma.
Similarities were noted between the nature of inner ear damage produced by loud sounds and by aminoglycoside antibiotics. Since body temperature affects cochlear function and influences the effects of noise on the ear, a similar effect was predicted for the aminoglycoside, kanamycin. By environmentally elevating the body temperatures of preweanling mice to approximately 1 degree C above that of the normal adult, kanamycin ototoxicity was increased (an average 20.4 dB threshold elevation, vs. 9.3 dB for kanamycin injected mice reared at room temperature). Hyperthermia per se had no influence on auditory thresholds. This may be of relevance to humans with fever who are treated with aminoglycoside antibiotics.
Surgical ligation of the external auditory canals of Mongolian gerbils produces aural cholesteatomas that are similar to spontaneous gerbilline cholesteatomas. These experimental cholesteatomas expand rapidly, medially displacing the tympanic membrane and eroding bone. Less than 2 months after ligation, half these cholesteatomas are in contact with the bony prominence of the cochlea. Ligation-induced formation of cholesteatomas may be unique to the gerbil. Keratin deposits are produced by similar ligations of the external auditory canals of cats, guinea pigs, hamsters, mice, and rats. However, in these animals there is no medial displacement of the tympanic membrane, no cholesteatoma formation, and no bone erosion. Cholesteatomas were not seen in cats, guinea pigs, hamsters, mice, and rats even after post-ligation intervals of 6 to 36 months.
The short latency (less then 10 ms) auditory nerve and brain stem evoked potentials of Jewett were examined in the inbred CBA/J laboratory mouse. Tone pips, at nine frequencies from 4 to 64 kHz, were used to determine auditory nerve evoked potential (P1) thresholds. Maximum sensitivity occurred at 32 kHz, and a second sensitive area was seen at 56 kHz. With the exception of 32 kHz, as stimulus frequencies were increased in octave intervals, the 90 dB P1 amplitude also increased. P1 latency decreased as the stimulus frequency was increased up to 32 kHz, but this trend reversed with further increases of frequency. However, the P1 amplitude-latency function produced a better agreement of latency and frequency with the travelling wave theory for amplitudes less than 1 micro V, while amplitudes from 2 to 8 micro V were independent of frequency. Latency and amplitude input-output functions for responses from the four auditory brain stem loci suggest that auditory information is differentially processed as a function of frequency at each level, This is especially true for the inferior colliculus, which is most sensitive to 8-KHz stimuli.
Auditory function of albino and pigmented gerbils was examined before and after treatment with the ototoxic aminoglycoside antibiotic gentamicin. Auditory brainstem responses (ABRs) and cochlear nerve compound action potentials (CAPs) were measured in response to pure tones having frequencies between 2 and 32 kHz. Age-matched albinos had significantly lower CAP, but not ABR, thresholds than pigmented gerbils. Gentamicin treatment elevated CAP and ABR thresholds in both genotypes, but pigmented gerbils were less severely affected. Compared to the ABR, the CAP is a more sensitive measure of ototoxicity and pigmentation differences. CAP tuning curves (TCs) were another sensitive measure of genotypic differences in susceptibility to ototoxicity. TC tip thresholds from pigmented animals given gentamicin were not as elevated as the TC tip thresholds of albinos.
Vocalizations often have periodic variations of their acoustic waveform envelope. Two simultaneously presented frequencies have an envelope fluctuation with a frequency equal to their difference tone (DT = F2-F1). Sinusoidal amplitude modulation (SAM) of a carrier frequency also produces an envelope fluctuation. Electrical ensemble responses to DT and SAM stimuli were recorded from the gerbil's round window. The predominant frequency of the response to the DT stimuli is F2-F1; to the SAM stimuli, it is the modulation frequency. Both responses are spectrally, temporally, and dynamically non-linear. Forward masking of a low-frequency DT response produced a tuning curve (TC) with a tip at the high-stimulus frequency. Forward masker TCs of a low-frequency SAM ensemble response had tips at the high frequency of the carrier. Tip thresholds and sharpness of tuning of DT and SAM TCs are quite similar, with cochlear neurons having high characteristic frequencies providing sharply tuned information about low frequency acoustic envelope periodicities.
Otosclerosis is an inherited disease in which abnormal bone growth results in ossicular fixation and hearing loss. Although the disease affects up to 10% of humans, it has not been observed in other animals. The LP/J inbred mouse has been found to develop abnormal bony lesions of the middle ear which resemble human otosclerosis. In this study of 113 temporal bones from LP/J mice, we found that the lesions develop after puberty and involve only the ossicles and the otic capsule. The most frequent site of involvement was the incus (46.9%), followed by the anterior crus of the stapes (31.3%), the malleus (14.2%), the otic capsule (14.2%), and the stapes footplate (8%). Cochlear hair cell loss was progressive throughout the lifespan of these animals. Although this disease is not identical in histologic appearance to human otosclerosis, understanding its disease process may shed light upon the pathophysiology of the human disease.
Volume-conducted, short-latency auditory-evoked potentials were examined in the laboratory mouse with lesions and local recording used to localize their sources. PI corresponds in time with N1 recorded from the round window, while isolation of the eighth cranial nerve from the brainstem results in the loss of all post-PI components. PII latency agrees with that of evoked potentials recorded from the cochlear nucleus. PIII latency corresponds with that of evoked potentials from the vicinity of the contralateral superior olivary nucleus, and lesions of this and closely related contralateral structures abolish PIII from the vertex recordings. PIV is reduced in amplitude by unilateral brainstem lesions between the superior olive and the inferior colliculus. Evoked potentials and lesions localized PV to the vicinity of the lateral regions of the contralateral inferior colliculus. PVI disappeared when areas anterior to the inferior colliculi were lesioned. Although minor species differences may exist, it was concluded that the sources for PI to V in the mouse closely resemble those in the cat, and they agree well with the limited data from the human. This technique may now be applied to studies of the numerous auditory mutants of the laboratory mouse.