本文選題：弓狀核 + NMDA受體　； 參考：《蘇州大學(xué)》2010年碩士論文

【摘要】：目的:本實驗旨在研究在外周炎癥時下丘腦弓狀核(hypothalamic arcuate nucleus, ARC)產(chǎn)生中樞敏感化及其谷氨酸受體機制和受體后信號轉(zhuǎn)導(dǎo)。 方法:建立完全弗氏佐劑(complete Freund’s adjuvant,CFA)炎癥痛模型;用玻璃微電極在體細胞外記錄ARC神經(jīng)元的自發(fā)放電及其對傷害性刺激的反應(yīng);側(cè)腦室內(nèi)微量注射MK-801(NMDA受體非競爭性拮抗劑)、Ro25-6981(NMDA受體NR2B亞單位拮抗劑)、CNQX(非NMDA受體拮抗劑)、PP2(Src家族蛋白酪氨酸激酶抑制劑)、GF109203X(蛋白激酶C抑制劑),觀察阻斷促離子型谷氨酸受體或受體后激酶磷酸化對正常大鼠及CFA炎癥大鼠ARC神經(jīng)元對傷害性刺激反應(yīng)的影響。 結(jié)果:(1)ARC神經(jīng)元的自發(fā)放電頻率,炎癥大鼠明顯高于正常大鼠;(2)ARC神經(jīng)元對傷害性刺激的反應(yīng),炎癥大鼠明顯高于正常大鼠;(3)側(cè)腦室內(nèi)微量注射MK-801(20nmol)、Ro25-6981(6nmol)、CNQX(20nmol)可抑制正常大鼠和炎癥大鼠ARC痛特異性神經(jīng)元對傷害性刺激的反應(yīng);(4)側(cè)腦室內(nèi)微量注射PP2(5nmol)、GF109203X(0.04nmol)可抑制正常大鼠和炎癥大鼠ARC痛特異性神經(jīng)元對傷害性刺激的反應(yīng)。 結(jié)論:(1)外周CFA炎癥時,ARC神經(jīng)元的興奮性提高,對傷害性刺激的反應(yīng)增強;(2)中樞NMDA受體及其NR2B亞單位、非NMDA受體參與正常大鼠和CFA炎癥大鼠ARC神經(jīng)元對傷害性刺激的反應(yīng);(3)腦內(nèi)Src蛋白酪氨酸激酶和蛋白激酶C可能參與正常大鼠和CFA炎癥大鼠ARC痛特異性神經(jīng)元對傷害性刺激的反應(yīng);(4)ARC作為脊髓以上水平調(diào)節(jié)痛覺的一個高位中樞,在外周炎癥時也可產(chǎn)生中樞敏感化。
[Abstract]:Aim: to study the central sensitization of hypothalamic arcuate nucleus in hypothalamic arcuate nucleus (Arc) and its glutamate receptor mechanism and postreceptor signal transduction during peripheral inflammation. Methods: the inflammatory pain model of complete Freund adjuvant complete Freund's adjuvant was established, and the spontaneous discharges of ARC neurons and their responses to nociceptive stimuli were recorded by glass microelectrode in vitro. Microinjection of MK-801(NMDA receptor noncompetitive antagonist Ro25-6981NMDA receptor NR2B subunit antagonist CNQXPP2Src family protein tyrosine kinase inhibitor PP2Src family protein tyrosine kinase inhibitor (protein kinase C inhibitor, protein kinase C) to observe the blocking of ion-promoting glutamate Effects of receptor or postreceptor kinase phosphorylation on nociceptive stimuli of ARC neurons in normal rats and CFA inflammatory rats. Results the frequency of spontaneous discharge of ARC neurons in 1: 1 was significantly higher in inflammatory rats than that in normal rats, and the responses to nociceptive stimuli in the neurons were significantly higher in the inflammatory rats than in the normal rats. Intraventricular microinjection of MK-801 / 20nmol (Ro25-6981nmol / 6nmol) inhibited the response of ARC pain-specific neurons to nociceptive stimuli in normal and inflammatory rats. The microinjection of PP25nmol-GF109203Xnmol in the lateral ventricle could inhibit inflammation and inflammation in normal and inflammatory rats. Response of ARC pain specific neurons to nociceptive stimuli in rats. Conclusion (1) the excitability and the response to nociceptive stimulation of CFA neurons increased during peripheral CFA inflammation. The central NMDA receptors and their NR2B subunits were also increased. The response of ARC neurons to nociceptive stimuli in normal rats and CFA inflammatory rats.) Src protein tyrosine kinase and protein kinase C in brain may be involved in ARC pain specific neurons in normal rats and CFA inflammatory rats. The response of noxious stimuli is that ARC serves as a high center for the regulation of pain sensation at the level above the spinal cord. Peripheral inflammation can also produce central sensitization.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2010
【分類號】：R364.5

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