本文關(guān)鍵詞：出生后環(huán)境依賴的大鼠聽皮層神經(jīng)元對聲刺激時間信息編碼的可塑性　出處：《華東師范大學(xué)》2016年博士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 大鼠 初級聽皮層 升降時間 間隔時程 噪聲暴露 豐富環(huán)境 純音暴露 可塑性

【摘要】：人的言語和動物的通訊聲中包含隨時間快速變化的幅度和頻率信息,聽覺系統(tǒng)對這些聲刺激中包含的時間信息的精確處理對人類的言語感知和動物的聲通訊至關(guān)重要。已有的研究表明,聽皮層對聲刺激包絡(luò)的升降時間以及聲刺激間隔時程等時間信息的編碼在出生后有一個發(fā)育的過程。出生后聽覺系統(tǒng)發(fā)育的過程中,聽皮層的功能具有環(huán)境和經(jīng)驗(yàn)依賴的可塑性,噪聲環(huán)境可導(dǎo)致聽皮層對聲刺激頻率、強(qiáng)度和空間方位等信息處理的缺陷,而豐富環(huán)境可增強(qiáng)大腦皮層的可塑性,并對聽皮層處理聲刺激頻率信息的缺陷有一定的修復(fù)作用。然而,出生后的環(huán)境如何影響聽皮層對聲刺激時間信息的處理尚未揭示清楚。本論文的目的是研究：1)出生后不同時期中等強(qiáng)度的噪聲暴露如何影響聽皮層對聲刺激時間信息的處理?2)如果噪聲暴露導(dǎo)致了聽皮層處理聲刺激時間信息的缺陷,豐富環(huán)境能否修復(fù)這種缺陷?為了回答這些問題,我們用胞外單細(xì)胞記錄技術(shù),研究出生后的不同環(huán)境對SD大鼠聽皮層神經(jīng)元編碼聲刺激包絡(luò)的升降時間信息和間隔時程信息的影響。本論文分為三部分,主要內(nèi)容包括：幼年和成年時期的噪聲暴露對大鼠聽皮層神經(jīng)元編碼聲刺激包絡(luò)的升降時間信息的影響實(shí)驗(yàn)在22只正常對照組、21只關(guān)鍵期噪聲暴露組以及20只成年噪聲暴露組大鼠上進(jìn)行。關(guān)鍵期噪聲暴露組大鼠在出生后10-31天隨母鼠飼養(yǎng)在70 dB SPL的白噪聲環(huán)境中,之后生活在正常環(huán)境下。成年噪聲暴露組大鼠在出生后57-77天飼養(yǎng)在噪聲環(huán)境中,正常對照組大鼠為飼養(yǎng)在正常環(huán)境下的同齡大鼠。所有大鼠在飼養(yǎng)到77天后進(jìn)行電生理實(shí)驗(yàn)。以聽皮層神經(jīng)元對純音刺激反應(yīng)的放電數(shù)(Number of spikes)和首次發(fā)放潛伏期(First spike latency)為研究對象,觀察神經(jīng)元的聽反應(yīng)如何隨聲刺激包絡(luò)的升降時間的變化而改變。結(jié)果發(fā)現(xiàn),當(dāng)聲刺激強(qiáng)度固定時,在所測定的升降時間條件下,關(guān)鍵期噪聲暴露組大鼠聽皮層神經(jīng)元的原始放電數(shù)以及標(biāo)準(zhǔn)化的放電數(shù)顯著低于其他兩組,其首次發(fā)放潛伏期以及潛伏期差值比其他兩組顯著延長。成年噪聲暴露組神經(jīng)元的原始放電數(shù)以及標(biāo)準(zhǔn)化的放電數(shù)與正常對照組無顯著差異,但其首次發(fā)放潛伏期以及潛伏期差值卻顯著大于正常對照組。聽覺發(fā)育關(guān)鍵期的噪聲暴露導(dǎo)致的潛伏期隨升降時間的變化率比成年時期的噪聲暴露大。這些結(jié)果提示,幼年和成年時期中等強(qiáng)度的噪聲暴露都對大鼠聽皮層神經(jīng)元處理聲刺激包絡(luò)的升降時間信息產(chǎn)生影響,但聽覺發(fā)育關(guān)鍵期噪聲暴露的影響比成年時期噪聲暴露的影響大。二、幼年和成年時期的噪聲暴露對大鼠聽皮層神經(jīng)元處理聲刺激間隔時程信息的影響實(shí)驗(yàn)在23只正常對照組、48只關(guān)鍵期噪聲暴露組以及28只成年噪聲暴露組大鼠上進(jìn)行。以聽皮層神經(jīng)元對不同間隔時程的序列聲刺激反應(yīng)的放電數(shù)和首次發(fā)放潛伏期為研究對象,觀察聽皮層神經(jīng)元對不同間隔時程條件下的聲刺激的反應(yīng),并分析神經(jīng)元對聲刺激間隔時程的探測閾值。結(jié)果發(fā)現(xiàn),與正常對照組相比,幼年時期的噪聲暴露導(dǎo)致大鼠在成年時聽皮層神經(jīng)元對聲刺激反應(yīng)的最低閾值的升高和首次發(fā)放潛伏期的延長,但成年時期的噪聲暴露只引起神經(jīng)元聽反應(yīng)潛伏期的延長,并未引起神經(jīng)元最低反應(yīng)閾值的顯著變化。幼年和成年時期中等強(qiáng)度的噪聲暴露均導(dǎo)致大鼠聽皮層神經(jīng)元對聲刺激間隔時程的探測閾值的升高,降低了聽皮層神經(jīng)元對聲刺激間隔時程信息的處理能力,但在幼年時期噪聲暴露的影響比在成年時期噪聲暴露的影響更大。三、豐富環(huán)境對幼年噪聲暴露導(dǎo)致的聽皮層神經(jīng)元對聲刺激間隔時程信息編碼缺陷的修復(fù)實(shí)驗(yàn)在24只豐富環(huán)境組大鼠,23只正常對照組大鼠,24只關(guān)鍵期噪聲暴露+豐富環(huán)境組大鼠,23只關(guān)鍵期噪聲暴露+純音暴露組大鼠上進(jìn)行。在出生后10-56天期間飼養(yǎng)于豐富環(huán)境中的大鼠(豐富環(huán)境組),其聽皮層神經(jīng)元的間隔探測閡值、最低反應(yīng)閾值、首次發(fā)放潛伏期等均與正常對照組大鼠無顯著差異。然而,如果將關(guān)鍵期噪聲暴露的大鼠立即置于豐富環(huán)境中飼養(yǎng)至成年(關(guān)鍵期噪聲暴露+豐富環(huán)境組),我們發(fā)現(xiàn)該組大鼠聽皮層神經(jīng)元的間隔探測閾值顯著低于關(guān)鍵期噪聲暴露組,這說明豐富環(huán)境飼養(yǎng)可以修復(fù)由于幼年噪聲暴露導(dǎo)致的神經(jīng)元對聲刺激間隔時程信息處理的缺陷。如果將經(jīng)過關(guān)鍵期噪聲暴露的大鼠只暴露于純音環(huán)境中(與豐富環(huán)境中的純音刺激相同)飼養(yǎng)至成年(關(guān)鍵期噪聲暴露+純音暴露組),該組大鼠聽皮層神經(jīng)元的間隔探測閾值比關(guān)鍵期噪聲暴露組低,但比關(guān)鍵期噪聲暴露+豐富環(huán)境組高,這說明豐富環(huán)境中的純音刺激對由于幼年噪聲暴露導(dǎo)致的神經(jīng)元對聲刺激間隔時程信息處理的缺陷有部分修復(fù)作用。本論文的研究結(jié)果表明,出生后聽覺發(fā)育關(guān)鍵期的噪聲暴露可導(dǎo)致聽皮層神經(jīng)元對聲刺激升降時間和聲刺激間隔時程信息處理的缺陷,豐富環(huán)境對幼年噪聲暴露誘導(dǎo)的聽皮層神經(jīng)元對聲刺激間隔時程信息處理的缺陷有修復(fù)作用。本研究為理解出生后環(huán)境依賴的聽覺中樞功能的可塑性提供了新的實(shí)驗(yàn)證據(jù),為聽覺中樞處理聲刺激時間信息缺陷的修復(fù)策略提供了實(shí)驗(yàn)依據(jù)和理論依據(jù)。
[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).
【學(xué)位授予單位】：華東師范大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：Q42
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本文編號：1344696