Auditory brain-stem evoked potentials in cat after kainic acid induced neuronal loss. II. Cochlear nucleus |
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| Affiliation: | 1. Institute of Artificial Intelligence & Cognitive Engineering, University of Groningen, Groningen, The Netherlands;2. Department of Psychology, University of Bern, Bern, Switzerland;3. Department of Psychology, Kent State University, Kent, OH, United States;4. Science for Monks, Palo Alto, CA, United States;5. Department of Psychiatry, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, United States;6. Zynerba Pharmaceuticals, Devon, PA, United States;7. Sera Jey Monastic University, Bylakuppe, India;8. Library of Tibetan Works and Archives, Dharamsala, India;9. Department of Psychological Sciences, Kent State University, Kent, OH, United States;1. Department of Vascular Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China;2. Key Laboratory of Molecular Medicine of Jiangxi Province, Nanchang, Jiangxi, China;3. Department of Laboratory Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China;2. Department of Environmental Science and Industrial Development, Faculty of Postgraduate Studies for Advanced Sciences, Beni-Suef University, Beni Suef, Egypt;6. Interdisciplinary Centre for Water Research, Indian Institute of Science, Bangalore, Karnataka, India;7. Department of Materials Engineering, Interdisciplinary Centre for Water Research, Indian Institute of Science, Bangalore, Karnataka, India;9. Department of Microbiology, Lovely Professional University, Punjab, India |
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| Abstract: | Auditory brain-stem potentials (ABRs) were studied in cats for up to 6 weeks after kainic acid had been injected unilaterally into the cochlear nucleus (CN) producing extensive neuronal destruction. The ABRcomponents were labeled by the polarity at the vertex (P, for positive) and their order of appearance (the arabic numerals 1,2, etc.). Component P1 can be further subdivided into 2 subcomponents, P1a and P1b. The assumed correspondence between the ABR components in cat and man is indicated by providing human Roman numeral designations in parentheses following the feline notation, e.g., P2 (III). To stimulation of the ear ipsilateral to the injection, the ABR changes consisted of a loss of components P2 (III) and P3 (IV), and an attenuation and prolongation of latency of components P4 (V) and P5 (VI). The sustained potential shift from which the components arose was not affected. Wave P1a (I) was also slightly but significantly attenuated compatible with changes of excitability of nerve VIII in the cochlea secondary to cochlear nucleus destruction. Unexpectedly, to stimulation of the ear contralateral to the injection side, waves P2 (III), P3 (IV), and P4 (V) were also attenuated and delayed in latency but to a lesser degree than to stimulation of the ear ipsilateral to the injection. Changes in binaural interaction of the ABR following cochlear nucleus lesions were similar to those produced in normal animals by introducing a temporal delay of the input to one ear. The results of the present set of studies using kainic acid to induce neuronla loss in auditory pathway when combined with prior lesion and recording experiments suggest that each of the components of the ABR requires the integrity of an anatomically diffuse system comprising a set of neurons, their axons, and the neurons on which they terminate. Disruption of any portion of the system will alter the amplitude and/or the latency of that component. |
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