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Biomedical subjects

G K Martin

Publications and source records attributed to G K Martin.

At least 73 records · Page 4Linked to original sources
PubMed1987

Acoustic distortion products in rabbit ear canal. II. Sites of origin revealed by suppression contours and pure-tone exposures.

Previous work on acoustic distortion products (DPs) recorded from the ear canal has not established unequivocally whether emitted DPs principally reflect basilar-membrane nonlinearities at the frequency sites of the primary tones, f1 and f2, or if the DP-frequency place itself makes a significant contribution to the emitted response. Results from some studies on acoustic emissions attribute generation of the emitted DP almost exclusively to the regions of maximum primary-tone interaction, while the findings of other investigations implicate reemission of the response from the DP locus as a significant contributor to response magnitude. Using suppression, interfering tones, and temporary threshold shift (TTS) procedures, the work reported here was designed to establish more definitively the precise contributions of the basilar-membrane regions involved in generating acoustic DPs in rabbits. Suppression tuning curves and interfering-tone experiments indicated that for the DP at 2f1-f2, regions near the f1 or f2 frequencies were the major contributors to the emitted response. However, for the higher-frequency DP at 2f2-f1, the basilar-membrane region just basal to the DP site was implicated as the generator. Following brief episodes of TTS at frequencies related to either the DP or the primary tones, the locus of the exposure stimulus that most effectively reduced the magnitude of the 2f1-f2 response also implicated the region of maximal primary-tone interaction in the generation of the acoustic DP. In contrast, for the DP at 2f2-f1, basilar-membrane sites nearer the DP were identified as the primary contributors to the emitted response. Both sets of results imply that different DPs recorded from the ear canal may originate from unique regions of primary-tone interaction along the basilar membrane.

Acoustic Stimulation↗
PubMed1987

Repeated TTS exposures in monkeys: alterations in hearing, cochlear structure, and single-unit thresholds.

The findings of a number of studies investigating the effects of excessive sound on hearing have indicated that the correspondence between behavioral, physiological, and histological measures of noise-induced hearing loss may be markedly dependent upon the sensitivity of the particular measure. Recent studies demonstrating significant changes in the responses of single auditory neurons following brief exposures to pure tones suggest that single-unit activity may be a sensitive indicator of physiological insult to the organ of Corti's sensory cells. In addition, the long-lasting nature of the changes in neural responsiveness suggests that each temporary threshold shift (TTS) episode may produce an increment of damage to the ear that eventually contributes to a measurable permanent threshold shift (PTS). A logical extension of this implication is the proposal that repeated episodes of TTS would first affect single-unit thresholds, and that such damage would eventually manifest itself as PTS. A test of this notion was performed by repeatedly exposing monkeys to short-lasting TTS sounds for many months. Behavioral thresholds were monitored using a reaction-time task before and after each inducement of TTS. Two subjects participated in exposure sessions for 18 months, while the remaining monkey was exposed to identical stimuli for 6 months. At the end of behavioral testing, the monkeys were prepared for chronic recording from single cells of the cochlear nucleus. Following the recording period, cochleas were prepared for examination as plastic-embedded whole mounts. Flat preparations of the cochlear duct were made and the position and extent of damage to the organ of Corti and myelinated nerve fibers were determined. No elevations in behavioral threshold were noted for the monkey receiving 6 months of sound-exposure experience, while for both subjects exposed for 18 months, a significant high-frequency hearing loss became apparent during the final months of exposure. For damaged ears, the thresholds of ipsilateral cochlear nucleus units were elevated for characteristic frequencies (CFs) corresponding to the frequency regions where behavioral thresholds were shifted. Thresholds for units with high-frequency CFs in the animal exposed for 6 months also demonstrated a loss in sensitivity. Histological examination of the cochleas of monkeys with permanent hearing losses revealed corresponding damage to the high-frequency region of the organ of Corti. The monkey exposed for 6 months, which demonstrated only elevated unit thresholds, also had high-frequency lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1986

Spontaneous, click-, and toneburst-evoked otoacoustic emissions from normal ears.

Evoked and spontaneous otoacoustic emissions were recorded bilaterally in a group of normal subjects (n = 14) using clicks and tonebursts at four frequencies (0.5, 1, 1.5, and 3 kHz). All ears (n = 28) demonstrated evoked emissions, but not to every stimulus type. The 0.5-kHz toneburst evoked emissions in only 10 (36%) ears, the 1.5-kHz toneburst in all ears, and the remaining stimuli in at least 80% of ears. Two distinct patterns of evoked emissions were identified. Five (18%) ears showed short, broadband click-evoked emissions lasting less than 20 ms after stimulus onset. In these ears, toneburst-evoked emissions were often more prominent than click-evoked emissions and no spontaneous emissions were detected. Twenty-three (82%) ears showed click-evoked emissions lasting longer than 20 ms poststimulus onset. Spectral analysis of these emissions demonstrated several (2-10) narrow frequency peaks. Highly similar peaks were present in the spectra of toneburst-evoked emissions within the range of toneburst spectra. Spontaneous emissions were recorded in 12 of the 23 ears. In these ears, at the frequencies of spontaneous emissions, prominent peaks in both click- and toneburst-evoked emission spectra were always present. Otoacoustic emission characteristics correlated significantly between the ears of individual subjects inferring that a symmetrical cochlear mechanism generates otoacoustic emissions.

Acoustic Stimulation↗
PubMed1985

Spontaneous otoacoustic emissions in the nonhuman primate: a survey.

A number of reports have described a relatively high incidence of spontaneous otoacoustic emissions (SOAEs) in recordings made from the sealed human ear canal. Our attempt to detect similar emissions in 122 presumably normal-hearing ears from 61 monkeys revealed SOAEs in 5% of the primates and 2.5% of the ears tested.

Animals↗
PubMed1984

Effects of reaction time performance on single-unit activity in the central auditory pathway of the rhesus macaque.

The activity of single units at various locations in the central auditory pathway of rhesus macaques was recorded during the monkeys' performance and nonperformance in an auditory reaction time task. Evoked unit responses during performance were compared with those observed during passive delivery of identical stimuli. Single units were recorded from the cochlear nucleus, superior olivary complex, lateral lemniscus, inferior colliculus, medial geniculate nucleus, and auditory cortex. Significant effects of task performance on unit discharge patterns were observed at all levels of the central auditory pathway: Spontaneous discharge rates in the more peripheral auditory nuclei tended to be higher during performance. Evoked discharge that occurred relatively late during a stimulus presentation (greater than 75 msec after stimulus onset) was increased during performance, compared with the nonperformance condition, in nuclei above the cochlear nucleus. The initial latency of evoked discharge was increased during performance for subcortical nuclei but was decreased for units in auditory cortex. These results suggest that the effects of performance may be mediated by a tonic increase in the excitability of auditory units which operates primarily at peripheral auditory stations, and a descending, stimulus-evoked increase in excitability which primarily influences the cells of higher auditory nuclei. At the cortical level, these changes lead to increased signal-to-noise ratio of the evoked response during performance in the auditory task.

Acoustic Stimulation↗
PubMed1983

Endolymphatic hydrops in the rabbit: auditory brainstem responses and cochlear morphology.

A rabbit model of endolymphatic hydrops was studied using detailed functional and cytohistologic methods. Immediately following surgical destruction of the endolymphatic sac and the distal portion of the duct, measures of the evoked auditory brainstem response (ABR) revealed mild to profound losses specific to low- and high-frequency test stimuli while responses to mid-frequency signals remained unchanged for the majority of animals. Rabbits exhibited varying degrees of vestibular upset involving both overt behavior and reduced responses to caloric stimulation. Histologic processing of the plastic embedded cochleae demonstrated distended Reissner's membranes along with extensive damage to apical and basal turn sensory cells and myelinated afferent nerve fibers while the middle portion of the cochlear duct remained relatively unaltered. An atypical pattern of hair cell lesions involving a greater loss for inner than for outer hair cells was identified at the interface between damaged apical sensorineural elements and the normal appearing organ of Corti of the middle turns.

Animals↗
PubMed1981

Temporary hearing loss from exposure to moderately intense tones in rhesus monkeys.

The amount and duration of temporary threshold shift produced by exposure to moderately loud sounds were quantitatively examined in rhesus monkeys using a simple, behavioral reaction-time procedure. Subjects were exposed to pure tones (100 dB SPL) either at the threshold test frequency or half an octave below (-1/2 OCT) the test frequency, usually for a duration of 3-minutes. Many features of the results were comparable to those observed in human subjects following exposure to similar sounds: (1) both the magnitude and the time course of recovery from the hearing loss were a function of the frequency and duration of the exposure stimulus with higher-frequency and longer-lasting stimuli producing greater threshold shifts and longer recovery time courses; (2) recovery time courses were monotonic and approximately exponential; (3) at low- and mid-frequency regions of hearing, intense stimulation at the test frequency and at -1/2 OCT produced similar threshold shifts and durations of recovery, while for high-frequency hearing -1/2 OCT stimuli always yielded greater losses and longer recovery periods; (4) although the peak hearing loss was either at , or a half octave above, the exposure frequency, the overall threshold-shift pattern was always assymmetrically distributed toward higher frequencies; (5) alterations in functions relating response latency to stimulus intensity were demonstrable. These psychophysical experiments form a framework that will permit further investigations into the physiologic basis of temporary threshold shift in an animal model highly similar to man.

Acoustic Stimulation↗
PubMed1980

A rabbit preparation for neuro-behavioral auditory research.

Auditory thresholds were determined in rabbits by a classically conditioned nicitating membrane response established with a tone-conditioned stimulus and a shock-unconditioned stimulus. The audiograms obtained were comparable in shape and sensitivity to threshold curves measured for a variety of small mammals by other conditioning techniques. This procedure provides a quick and efficient method for measuring hearing sensitivity in a restrained preparation that permits precise stimulus control as well as providing an ideal situation for a variety of physiological studies of hearing in an awake, behaving animal.

Animals↗
PubMed1980

Classical conditioning of the rabbit (Oryctolagus cuniculus) nictitating membrane response, with electrical brain stimulation as the unconditioned stimulus.

Rabbits were given classical conditioning training by using paired tone CS (conditioned stimulus) and brain-shock UCS (unconditioned stimulus), with the stimulating electrode localized in the vicinity of the abducens (6th nerve) nucleus such that the electrical stimulus elicited a low-threshold nictitating membrane (NM) extension response as the unconditioned response. Eight of the 27 animals developed clear conditioned NM responses to the tone CS. Control procedures, e.g., subsequent explicity unpaired training, argue against sensitization, pseudoconditioning, and "kindling" as possible explanations. There was no clear-cut anatomical differentiation of electrode-tip locations between learners and nonlearners. Both learners and nonlearners were subsequently trained with paired tone-corneal air puff, and neuronal unit activity was recorded from the stimulating electrode. Animals that had learned with the prior brain-shock UCS exhibited substantially greater increases in neuronal unit activity during air-puff training, which suggests the existence of a differentially effective anatomical-physiological substrate for conditionability.

Abducens Nerve↗