博士 / 高雄醫學院 / 醫學研究所 / 87 / Hearing system is the main route by which the animals perceive message in auditory sense. Apart from ascending and descending pathways, there are two feedback systems in the auditory brain that protect the mammals from excessive noise. The first one is the middle—ear muscle reflex and the other system is the olivocochlear efferent system that is originated from the superior olivary complex and projecting towards the cochlea named olivocochlear bundle (OCB). Most of literatures reported that OCB could inhibit the activities and excitation of outer hair cells and auditory nerve so reduce the overstimulation of inner ear and then protect from hearing damage.
Hearing is an important sensory input to an animal, hence a hearing impaired animal would exhibit modified behavior compared with a hearing intact animal. Scarce literatures had been devoted to the study of such modified behavior in hearing impaired animal. Thus, this thesis is aimed to study the changes of the animals whose OCB has been demolished by radiofrequency current after stereostaxis. In the present studies, electrophysiological methods, long-term locomotor activity monitoring and Fos immunohistochemistry (early gene c-Fos) shall be used to examine and to provide evidences of OCB actions in central auditory system during acute, chronic effects and protective role under noise exposure.
Brainstem auditory evoked potential (BAEP), as the name implies, records the electrical potentials of the ascending auditory pathway during the first 10ms after external stimulus and it reflects the auditory related neuronal activity in the brainstem. This method was used to record the changes took placed after OCB lesion of rats. The results showed no significant changes in the BAEP peak latencies could be observed but the BAEP amplitudes from waves I to III were increased significantly. It meant that the suppressed effect of OCB was removed from ascending pathway and cochlear nucleus, hence leading to the increase in numbers of neurons that discharge action potentials and the increased BAEP amplitudes reflected such neuronal hyperactivity. Meanwhile, long-term locomotor activity monitoring recorded an increased activity of the OCB-lesion rat especially exploring and stereotype behaviors. We hypothesized that the impaired OCB not long imposed an inhibitory effect on the hearing so the animals perceived more external stimuli than before and this reflected on the increased in exploring and locomotor activities. Apart from the electrophysiological study, tone-evoked expression of early gene c-fos could also provide direct evidence at molecular level of the consequences before and after the OCB was disrupted. The Fos immunohistochemical study showed that tone-evoked Fos-like immunoreactivity was present in auditory neurons of OCB-lesion, sham-operated and normal rats under no noise exposure. After moderate-intensity noise exposure for 5 days, the Fos only appeared in sham-operated and normal groups but not in OCB-lesion group. The hearing threshold levels were all increased in three groups especially the OCB-lesion group. The Fos all disappeared in three groups of rats after continuations of 10-day moderate-level or high-level noise exposure following 10-day moderate-level noise exposure. This signified that while the OCB was lesioned, the auditory system would be more vulnerable and a further increased in hearing thresholds that would cause Fos induction impossible and difficult.
Due to the importance of OCB in electrophysiology and locomotor activity, interests were aroused in seeking possible connection between OCB lesion and tinnitus. Tinnitus is a disturbing symptom with poorly understood etiology and mechanism. The majority of literatures suggest that the disinhibition after OCB was damaged would allow the OHC to continue firing hence leading to hyper-responsiveness of auditory afferents and was the possible generation of tinnitus. One aspect in our studies is to compare our OCB lesion animal model with the popular established model that is postulated by aspirin (salicylate) injection. We replicated the aspirin-induced tinnitus animal model, also measured the BAEP and recorded the locomotor activity and then compared with the OCB-lesion rats to find if there were any comparable observations. The results showed that the BAEP latencies were decreased but amplitude was no changes 80 minutes after aspirin injection. In the OCB-lesion model, the BAEP amplitudes were enlarged without latency delay. Locomotor activity monitoring provided other measurement after aspirin injection. The locomotor activity of the rat decreased significantly after aspirin injection but the OCB-lesion rat exhibited increased locomotor activity. All the aforementioned data indicated that aspirin-injection and OCB-lesion groups would produce substantially different results. Hence we proposed that tinnitus would not be produced at all after the OCB was damaged, or at a wilder sense, the two ways of eliciting tinnitus were so radically different that resulted in two distinctive different responses of animals. In conclusion, this thesis confirms that the OCB lesion and the aspirin-induced tinnitus animal models were in fact different models and shall not be replaced.
| Identifer | oai:union.ndltd.org:TW/087KMC00534007 |
| Date | January 1999 |
| Creators | Yueh-Ling Hsieh, 謝悅齡 |
| Contributors | Tsan-Ju Chen, Shun-Sheng Chen, 陳 贊 如, 陳 順 勝 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 118 |
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