出生后环境依赖的大鼠听皮层神经元对声刺激时间信息编码的可塑性

发布时间：2017-12-28 05:13

  本文关键词：出生后环境依赖的大鼠听皮层神经元对声刺激时间信息编码的可塑性　出处：《华东师范大学》2016年博士论文　论文类型：学位论文

  更多相关文章： 大鼠 初级听皮层 升降时间 间隔时程 噪声暴露 丰富环境 纯音暴露 可塑性

【摘要】：人的言语和动物的通讯声中包含随时间快速变化的幅度和频率信息,听觉系统对这些声刺激中包含的时间信息的精确处理对人类的言语感知和动物的声通讯至关重要。已有的研究表明,听皮层对声刺激包络的升降时间以及声刺激间隔时程等时间信息的编码在出生后有一个发育的过程。出生后听觉系统发育的过程中,听皮层的功能具有环境和经验依赖的可塑性,噪声环境可导致听皮层对声刺激频率、强度和空间方位等信息处理的缺陷,而丰富环境可增强大脑皮层的可塑性,并对听皮层处理声刺激频率信息的缺陷有一定的修复作用。然而,出生后的环境如何影响听皮层对声刺激时间信息的处理尚未揭示清楚。本论文的目的是研究：1)出生后不同时期中等强度的噪声暴露如何影响听皮层对声刺激时间信息的处理?2)如果噪声暴露导致了听皮层处理声刺激时间信息的缺陷,丰富环境能否修复这种缺陷?为了回答这些问题,我们用胞外单细胞记录技术,研究出生后的不同环境对SD大鼠听皮层神经元编码声刺激包络的升降时间信息和间隔时程信息的影响。本论文分为三部分,主要内容包括：幼年和成年时期的噪声暴露对大鼠听皮层神经元编码声刺激包络的升降时间信息的影响实验在22只正常对照组、21只关键期噪声暴露组以及20只成年噪声暴露组大鼠上进行。关键期噪声暴露组大鼠在出生后10-31天随母鼠饲养在70 dB SPL的白噪声环境中,之后生活在正常环境下。成年噪声暴露组大鼠在出生后57-77天饲养在噪声环境中,正常对照组大鼠为饲养在正常环境下的同龄大鼠。所有大鼠在饲养到77天后进行电生理实验。以听皮层神经元对纯音刺激反应的放电数(Number of spikes)和首次发放潜伏期(First spike latency)为研究对象,观察神经元的听反应如何随声刺激包络的升降时间的变化而改变。结果发现,当声刺激强度固定时,在所测定的升降时间条件下,关键期噪声暴露组大鼠听皮层神经元的原始放电数以及标准化的放电数显著低于其他两组,其首次发放潜伏期以及潜伏期差值比其他两组显著延长。成年噪声暴露组神经元的原始放电数以及标准化的放电数与正常对照组无显著差异,但其首次发放潜伏期以及潜伏期差值却显著大于正常对照组。听觉发育关键期的噪声暴露导致的潜伏期随升降时间的变化率比成年时期的噪声暴露大。这些结果提示,幼年和成年时期中等强度的噪声暴露都对大鼠听皮层神经元处理声刺激包络的升降时间信息产生影响,但听觉发育关键期噪声暴露的影响比成年时期噪声暴露的影响大。二、幼年和成年时期的噪声暴露对大鼠听皮层神经元处理声刺激间隔时程信息的影响实验在23只正常对照组、48只关键期噪声暴露组以及28只成年噪声暴露组大鼠上进行。以听皮层神经元对不同间隔时程的序列声刺激反应的放电数和首次发放潜伏期为研究对象,观察听皮层神经元对不同间隔时程条件下的声刺激的反应,并分析神经元对声刺激间隔时程的探测阈值。结果发现,与正常对照组相比,幼年时期的噪声暴露导致大鼠在成年时听皮层神经元对声刺激反应的最低阈值的升高和首次发放潜伏期的延长,但成年时期的噪声暴露只引起神经元听反应潜伏期的延长,并未引起神经元最低反应阈值的显著变化。幼年和成年时期中等强度的噪声暴露均导致大鼠听皮层神经元对声刺激间隔时程的探测阈值的升高,降低了听皮层神经元对声刺激间隔时程信息的处理能力,但在幼年时期噪声暴露的影响比在成年时期噪声暴露的影响更大。三、丰富环境对幼年噪声暴露导致的听皮层神经元对声刺激间隔时程信息编码缺陷的修复实验在24只丰富环境组大鼠,23只正常对照组大鼠,24只关键期噪声暴露+丰富环境组大鼠,23只关键期噪声暴露+纯音暴露组大鼠上进行。在出生后10-56天期间饲养于丰富环境中的大鼠(丰富环境组),其听皮层神经元的间隔探测阂值、最低反应阈值、首次发放潜伏期等均与正常对照组大鼠无显著差异。然而,如果将关键期噪声暴露的大鼠立即置于丰富环境中饲养至成年(关键期噪声暴露+丰富环境组),我们发现该组大鼠听皮层神经元的间隔探测阈值显著低于关键期噪声暴露组,这说明丰富环境饲养可以修复由于幼年噪声暴露导致的神经元对声刺激间隔时程信息处理的缺陷。如果将经过关键期噪声暴露的大鼠只暴露于纯音环境中(与丰富环境中的纯音刺激相同)饲养至成年(关键期噪声暴露+纯音暴露组),该组大鼠听皮层神经元的间隔探测阈值比关键期噪声暴露组低,但比关键期噪声暴露+丰富环境组高,这说明丰富环境中的纯音刺激对由于幼年噪声暴露导致的神经元对声刺激间隔时程信息处理的缺陷有部分修复作用。本论文的研究结果表明,出生后听觉发育关键期的噪声暴露可导致听皮层神经元对声刺激升降时间和声刺激间隔时程信息处理的缺陷,丰富环境对幼年噪声暴露诱导的听皮层神经元对声刺激间隔时程信息处理的缺陷有修复作用。本研究为理解出生后环境依赖的听觉中枢功能的可塑性提供了新的实验证据,为听觉中枢处理声刺激时间信息缺陷的修复策略提供了实验依据和理论依据。
[Abstract]:Human speech and animal communication contain information about amplitude and frequency that changes rapidly over time. The accurate processing of auditory information contained in these stimuli is crucial for human speech perception and animal voice communication. Previous studies have shown that auditory cortex has a developmental process for the time of ascending and falling time of the stimulus and interval information of interval intervals. The process of postnatal development of auditory system, the auditory cortex has the function of environment and experience dependent plasticity, noise can lead to defects in the auditory cortex sound stimulation frequency, intensity and spatial information processing, and the enriched environment can enhance the plasticity of the cerebral cortex, and the auditory cortex defect acoustic stimulation frequency information processing have the function of repair. However, how the postnatal environment affects the processing of auditory cortex for sound stimulation has not been revealed. The purpose of this paper is to study: 1) noise in different periods of moderate intensity exposure affects the auditory cortex to acoustic stimulation time information after birth? 2) if leads to defects listen to cortical processing acoustic stimulation time information noise exposure, enriched environment can repair this defect? In order to answer these questions, we used extracellular single cell recording technique of different environment after birth to investigate the effects of information envelope fall time information and interval encoding of acoustic stimulation in the cortical neurons of SD rats. This paper is divided into three parts, the main contents include: the noise of juvenile and adult period of exposure to the lifting time information envelope of cortical neurons encoding sound stimulation effects in 22 normal control group, 21 rats during the critical period of noise exposure group and 20 adult noise exposure group rats in rats. The critical period of noise exposure group rats were 10-31 days after their mother were reared in white noise is 70 dB SPL, after living in a normal environment. The rats in the adult noise exposure group were raised in the noise environment 57-77 days after birth, and the normal control group was the same age rats in the normal environment. All rats were reared after 77 days of electrophysiological experiments. The number of auditory neurons (Number of spikes) and the first First latency (First spike latency) of auditory cortex neurons were observed. Results show that when the sound stimulus intensity is fixed, the lifting time determined under the conditions, the critical period of noise exposure group in rat auditory cortical neurons discharge number and the number of the original discharge standard was significantly lower than that of the other two groups, the first spike latency and latency difference significantly longer than two other groups. There was no significant difference in the number of neurons in the adult noise exposure group and the normalized number of discharges, but the latency and latency difference in the first time were significantly higher than those in the normal control group. Noise exposure in the critical stage of auditory development resulted in a greater change in the latency than the noise exposure in the adult period. These results suggest that moderate intensity noise exposure during childhood and adulthood can influence the ascending and falling time information of auditory cortex processing in rats, but the influence of noise exposure during the critical period of auditory development is greater than that of adult exposure. Two, the effects of noise exposure during childhood and adulthood on the interval time information of auditory cortex in rats were analyzed in 23 normal control group, 48 critical period noise exposure group and 28 adult noise exposure group. To discharge to the sound sequence on cortical neuron different interval duration stimuli and first spike latencies as the research object, observe the auditory cortex neurons in different time interval under the condition of acoustic stimuli, and analysis of detection threshold neurons to acoustic stimulus interval duration. The results showed that compared with normal control group, childhood exposure to noise rat auditory cortical neurons increased to the minimum threshold sound stimuli and first spike latency prolonged in adulthood, but the noise of adult exposure caused only to neurons prolonged reaction latency, did not cause significant changes in the minimum threshold neuron response. The noise of juvenile and adult period of moderate intensity exposure resulted in increased detection threshold cortical neurons to sound stimulus interval duration of rats to reduce the processing capacity, listen to cortical neurons to sound stimulus interval time history information, but in the influence of childhood exposure to noise ratio in the effects of noise exposure during more years. Three, enrich the environmental exposure of auditory cortical neurons to acoustic stimulus interval duration information encoding defect repair experiments in 24 rats of early enriched environment noise, 23 normal control rats, 24 rats during the critical period of exposure to noise + enriched environment group rats, 23 rats during the critical period of noise exposure and pure tone exposure a group of rats. In 10-56 days after birth period reared in enriched environment rats (enriched environment group), the auditory cortex neurons of the interval detection threshold value and minimum response threshold and first spike latencies were compared with normal control rats had no significant difference. However, if the critical period of noise exposure in rats immediately in enriched environment reared to adulthood (critical period of noise exposure and enriched environment group), we found that the cortical neurons of the gap detection thresholds were significantly lower than the critical period of noise exposure group, the rats were listening, indicating that the rich environment could be restored because of noise exposure in childhood neurons to acoustic stimulation time interval defect information processing. If the rats exposed to critical period noise were exposed to pure tone environment (same as pure tone stimuli in the rich environment), they were raised to adult (critical period noise exposure + pure tone exposure group).
【学位授予单位】：华东师范大学
【学位级别】：博士
【学位授予年份】：2016
【分类号】：Q42
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本文编号：1344696