Kayla Minesinger , Maria Fernanda Yepes , Suhrud M. Rajguru
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In this study, we serially compare cochlear function in rats exposed to hazardous noise to induce noise-induced hearing loss (NIHL) under the effects of either ketamine or telazol. Awake male Brown Norway rats were exposed to octave band noise (4–8 kHz) at 110 dB SPL for 1 h. Cochlear function was assessed over multiple time points using either intramuscular injection of ketamine (44 mg/kg) and xylazine (5 mg/kg) or intraperitoneally injected telazol (20 mg/kg) and xylazine (5 mg/kg). Changes in ABR threshold, latency, and amplitude were compared to baseline<!--> <!-->(pre-NIHL) over 28 days. Functional results demonstrated that both ketamine- and telazol-anesthetized animals experience permanent changes in thresholds following noise. While both amplitude and latency were affected by noise, there were no significant differences in the changes between ketamine and telazol groups. 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引用次数: 0
摘要
研究表明,在研究外周听觉系统创伤相关变化的啮齿动物模型中,麻醉可以影响听觉脑干反应(ABR)等标准功能测试的结果。在临床前模型评估中,麻醉剂也可能混淆潜在疗法的效果。氯胺酮是一种n -甲基- d -天冬氨酸(NMDA)受体拮抗剂,是啮齿动物模型中常用的麻醉剂。研究表明,与其他麻醉剂不同,氯胺酮对ABR测量的影响很小。替乐胺是一种化学上类似氯胺酮的化合物,也是一种NMDA拮抗剂。替乐胺与唑拉西泮(特拉唑)联合使用,由于其副作用较轻且长效,可能是氯胺酮的替代品。在本研究中,我们在氯胺酮和特拉唑的作用下,对暴露于有害噪声诱导的噪声性听力损失(NIHL)大鼠的耳蜗功能进行了连续比较。将醒着的雄性褐挪威大鼠暴露于110 dB SPL的4-8 kHz的倍频噪声中1 h。通过肌肉注射氯胺酮(44 mg/kg)和噻嗪(5 mg/kg)或腹腔注射替拉唑(20 mg/kg)和噻嗪(5 mg/kg),在多个时间点评估耳蜗功能。将ABR阈值、潜伏期和幅度的变化与基线(nihl前)在28 天内进行比较。功能结果表明,氯胺酮和泰拉唑麻醉的动物在噪音后的阈值都经历了永久性的变化。虽然振幅和潜伏期都受到噪声的影响,但氯胺酮组和特拉唑组之间的变化无显著差异。我们的研究结果表明,特拉唑的行为与氯胺酮相似,可以作为啮齿动物模型实验中评估噪音创伤后听力敏感性的替代方法。
Comparison of actions of ketamine and telazol on cochlear function in a rodent model of noise-induced hearing loss
Research has shown that anesthesia used in rodent models studying trauma-related changes in the peripheral auditory system can impact the results of standard functional tests like the auditory brainstem response (ABR). The anesthetic agents may also confound the effects of potential therapeutics under evaluation in the preclinical models. Ketamine, a N-methyl-D-aspartate (NMDA) receptor antagonist, is a commonly employed anesthetic in rodent models. Studies have shown that ketamine, unlike other anesthetics, exerts minimal effects on ABR measurements. Tiletamine, a compound chemically akin to ketamine, is also an NMDA antagonist. Tiletamine combined with zolazepam (Telazol) may be a substitute for ketamine given its less severe side-effects and long-acting capacity. In this study, we serially compare cochlear function in rats exposed to hazardous noise to induce noise-induced hearing loss (NIHL) under the effects of either ketamine or telazol. Awake male Brown Norway rats were exposed to octave band noise (4–8 kHz) at 110 dB SPL for 1 h. Cochlear function was assessed over multiple time points using either intramuscular injection of ketamine (44 mg/kg) and xylazine (5 mg/kg) or intraperitoneally injected telazol (20 mg/kg) and xylazine (5 mg/kg). Changes in ABR threshold, latency, and amplitude were compared to baseline (pre-NIHL) over 28 days. Functional results demonstrated that both ketamine- and telazol-anesthetized animals experience permanent changes in thresholds following noise. While both amplitude and latency were affected by noise, there were no significant differences in the changes between ketamine and telazol groups. Our findings suggest that telazol behaves similarly to ketamine and could be an alternative in rodent model experiments for the evaluations of hearing sensitivity following noise trauma.
期刊介绍:
An international multidisciplinary journal devoted to fundamental research in the brain sciences.
Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed.
With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.