單側(cè)黑質(zhì)紋狀體通路損毀改變大鼠丘腦網(wǎng)狀核神經(jīng)元的電活動(dòng).doc

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1、單側(cè)黑質(zhì)紋狀體通路損毀改變大鼠丘腦網(wǎng)狀核神經(jīng)元的電活動(dòng)作者：張巧俊　劉健　劉婭萍　袁海峰　高蕊　向莉【摘要】　　目的觀察單側(cè)黑質(zhì)紋狀體通路損毀對(duì)大鼠丘腦網(wǎng)狀核神經(jīng)元電活動(dòng)的影響。方法采用在體細(xì)胞外記錄方法研究正常大鼠和帕金森病(Parkinson’sdisease,PD)模型大鼠丘腦網(wǎng)狀核(TRN)γ氨基丁酸(GABA)能神經(jīng)元放電頻率和放電形式的變化。結(jié)果對(duì)照組和PD組大鼠TRN神經(jīng)元的放電頻率分別是(14.7±1.6)Hz(n=23)和(33.8±3.0)Hz(n=29)，PD組大鼠TRN神經(jīng)元的放電頻率顯著高于對(duì)照組(P<0.001)。在對(duì)照組大鼠，17%的神經(jīng)元呈現(xiàn)不規(guī)則放

2、電，83%為爆發(fā)式放電；而在PD組大鼠，具有規(guī)則、不規(guī)則和爆發(fā)式放電的神經(jīng)元比例分別為7%、45%和48%，爆發(fā)式放電的神經(jīng)元比例明顯低于對(duì)照組(P<0.05)。結(jié)論單側(cè)黑質(zhì)紋狀體通路損毀誘發(fā)大鼠TRN內(nèi)GABA能神經(jīng)元的放電頻率增高，爆發(fā)式放電減少，這種變化可能與皮質(zhì)TRN興奮性神經(jīng)傳遞增強(qiáng)和蒼白球TRN抑制性神經(jīng)傳遞減弱有關(guān)?！娟P(guān)鍵詞】丘腦網(wǎng)狀核；帕金森?。沪锚舶被∷?；電生理學(xué)；大鼠　　Unilaterallesionofthenigrostriatalpathwaychangestheneuronalactivity　ofthereticularthalamicnucle

3、usintherat　　ABSTRACT:ObjectiveToinvestingatethechangesinneuronalactivityofthethalamicreticularnucleus(TRN)followingtheunilaterallesionofthenigrostriatalpathway.MethodsThechangesinthefiringrateandfiringpatternoftheTRNGABAergicneuronswereexaminedwithextracellularrecordingmethodsincontrolandParkinson

4、sdisease(PD)rats.ResultsTheresultsshowedthatthefiringratesofTRNneuronsincontrolandPDratswere14.7±1.6Hz(n=23)and33.8±3.0Hz(n=29),respectively,andthefiringrateofTRNneuronsinPDratswassignificantlyincreasedwhencomparedtothatofcontrolrats(P<0.001).Incontrolrats,17%oftheneuronsfiredirregularlyand83%

5、inbursts.InPDrats,7%oftheneuronsfiredregularly,45%irregularlyand48%inbursts,thepercentageoftheneuronsfiringinburstsbeingsiginificantlowerthanthatofcontrolrats(P<0.05).ConclusionUnilaterallesionofthenigrostiatalpathwayinducesanincreaseofthefiringrateontheTRNGABAergicneuronsandadecreaseoftheperce

6、ntageoftheneuronsfiringinbursts,suggestingthatthechangesmaybeassociatedwiththeincreaseofthecorticalTRNexcitatoryneurotransmissionanddecreaseoftheglobuspallidusTRNinhibitoryneurotransmission.6　　KEYWORDS:thalamicreticularnucleus;Parkinsonsdisease;γaminobutyricacid;electrophysiology;rat　　丘腦網(wǎng)狀核(th

7、alamicreticularnucleus,TRN)位于背側(cè)丘腦的前外側(cè)面，主要由γ–氨基丁酸(γaminobutyricacid,GABA)能神經(jīng)元組成，與丘腦、皮質(zhì)有廣泛的纖維聯(lián)系。因此，TRN影響丘腦和皮層之間的神經(jīng)信息傳遞，參與感覺、運(yùn)動(dòng)和邊緣系統(tǒng)功能活動(dòng)的調(diào)節(jié)[1]。研究發(fā)現(xiàn)TRN與帕金森病(Parkinson’sdisease,PD)的靜止性震顫有密切關(guān)系。TRN也接受來自基底神經(jīng)節(jié)的纖維投射，特別是來自