实验性局灶性脑缺血再灌注Fos蛋白的表达

目的　探讨大鼠局灶性脑缺血再灌注Fos蛋白表达的意义及其机制。方法　采用免疫组化法观察Fos蛋白在大鼠局灶性脑缺血再灌注后皮层和基底节区的动态变化。结果　Fos蛋白在大脑中动脉阻断 1h后 ,随再灌注时间延长其分布不同。基底节区持续时间长 ,阳性细胞多 ,而皮层持续时间短 ,阳性细胞少。其中再灌注 90min ,Fos蛋白表达最显著。大脑中动脉供血中心区皮层几无表达。结论　Fos蛋白的表达与神经细胞存活密切相关 ,出现Fos蛋白表达的区域神经元易于耐受缺血性损害而存活 ,可能是神经细胞自我保护机制之一 ,Fos蛋白的表达存在扩散抑制     

实验性瞬时高血压诱发大鼠脑内Fos表达

目的：观察大鼠中枢神经系统调节血压的部位,和苯肾上腺素静脉注射制作大鼠高血压模型,以抗Ｆｏｓ蛋白免疫组织化学方法,观察全脑Ｆｏｓ阳性神经元分布。结果高血压诱发下列区域Ｆｏｓ阳性细胞集中分布：延髓内脏带、臂旁外侧核、室核、视上核,杏仁核、终纹床核、额皮质１,２区、扣带皮质及梨状前皮质。位于延髓内脏带孤束核内的Ａ２细胞群和腹外侧区的Ａ１细胞群分别有３７．６３％和５４．２５％的酪氨酸羟化酶阳性神经元表达     

大鼠脑出血后延髓内脏带内儿茶酚胺能神经元的Fos表达

目的 观察大鼠脑出血后延髓内脏带儿茶酚胺能神经元的Ｆｏｓ表达。方法 尾壳核局部注射胶原酶制作脑出血模型,用抗Ｆｏｓ蛋白和抗酪氨酸羟化酶（ＴＨ）的双重免疫组织化学方法（ＡＢＣ法）,观察延髓内脏带内Ｆｏｓ蛋白表达及其与ＴＨ阳性神经元的共存。结果 有大量的Ｆｏｓ阳性细胞出现在延髓内,它们主要局限在延髓内脏带内,并以孤束核（ＮＴＳ）与延髓腹外侧区（ＶＬＭ）较为密集。ＮＴＳ和ＶＬＭ内Ｆｏｓ／ＴＨ双标细胞占Ｔ     

非NMDA受体拮抗剂对大鼠牙髓伤害性刺激诱导的延髓Fos表达

目的 研究兴奋性氨基酸非ＮＭＤＡ受体在牙髓伤害性信息传递中的作用,为揭示牙痛的产生机制打下基础。方法 将实验动物随机分为４组。第１组单纯给予机械穿髓刺激;第２组预先侧脑室注射非ＮＭＤＡ受体拮抗剂ＣＮＱＸ,再给予相同的穿髓刺激;第３组只行ＣＮＱＸ侧脑室注射,不予穿髓刺激;第４组为正常对照组。动物存活相同时间后取延髓做Ｆｏｓ蛋白免疫组化反应。观察３组动物Ｆｏｓ免疫反应阳性细胞的数量与第１组比较没有显著     

Brainstem catecholaminergic neurons activated by hypoxemia express GR and are coordinately activated with fetal sheep hypothalamic paraventricular CRH neurons

In late gestation, challenges to fetal homeostasis are accompanied by increases in adrenocorticotropin (ACTH) concentrations in fetal peripheral plasma and Fos (c-fos protein) activation in corticotropin-releasing hormone (CRH) neurons of the fetal hypothalamic paraventricular nucleus (PVN). In adults, ventrolateral brainstem catecholaminergic (CA) neurons (A1/C1, A2/C2) project to the parvocellular neurons of the PVN, possess glucocorticoid receptors (GR) and are Fos activated in parallel with CRH neurons of the PVN during hypoxia. Such observations suggest a role for the aforementioned medullary neurons in the function of the hypothalamo-pituitary-adrenal axis. The present study utilized late gestation fetal sheep, stereotaxic methodology and retrograde axon tracing and immunocytochemical techniques to investigate the relationship between activation of fetal brainstem CA neurons and activation of fetal PVN CRH immunopositive neurons in response to hypoxemia. Results indicated that: (1) the largest brainstem CA projection to PVN CRH neurons is from A1/C1 neurons, (2) brainstem neurons exhibit GR immunostaining and (3) brainstem CA neurons show a strong correlation (A1/C1 - r(2)=0.894, P<0.005; A2/C2 - r(2)=0. 848; P<0.002) of Fos activation with Fos activation in PVN CRH cells. We conclude that in late gestation the brainstem A1/C1 and A2/C2 areas are in position to influence the function of the hypothalamo-pituitary-adrenal axis during hypoxemic challenges to homeostasis in a fashion similar to that which has been demonstrated in the adult rat.     

Fos induction in the brain of mice exhibiting behavioral abnormalities following administration of allylnitrile or crotononitrile

Allylnitrile and crotononitrile induce behavioral abnormalities in mice. To explore the possible involvement of the vestibular system in these behavioral abnormalities, the expression of Fos protein, used as an indicator of neuronal activity, was examined within various brain structures in allylnitrile-, crotononitrile- and vehicle-treated mice. In each nitrile-treated mouse, Fos expression was observed in brain structures, which were divided into two groups. The structures in group 1 showed Fos expression between 1.5 h and 2 days postdosings, and in those in group 2 expression remained for up to 30 days postdosing. As most of these structures, especially in group 2, were identical to some Fos-positive structures observed after unilabyrinthectomy, the present results indicate that each nitrile induces Fos expression by causing a change in the peripheral vestibular system, resulting in behavioral abnormalities.     

CNQX对伤害性刺激隐神经诱发大鼠脊髓Fos蛋白表达的影响

目的 探讨伤害性刺激隐神经（SN）能否诱发脊髓神经元Fos蛋白表达及发生机制.方法 应用免疫组化方法观察伤害性刺激SN和尾静脉注射谷氨酸非NMDA受体拮抗剂（CNQX）后诱发脊髓神经元Fos蛋白表达的变化.结果 伤害性刺激SN后,诱导脊髓神经元Fos蛋白表达显著增强,CNQX拮抗了Fos蛋白表达的显著增强.结论 以伤害性刺激SN模拟躯体痛后,CNQX拮抗了伤害性刺激SN引起的脊髓神经元Fos蛋白表达的显著增加,表明非NMDA受体在躯体痛的调控中起到了重要的作用.     

大鼠孤束核内H3受体对哮喘发作时脑组织中Fos蛋白表达的影响

目的:探讨大鼠孤束核(NTS)内组胺H3受体对哮喘发作时大脑Fos蛋白表达的影响及其意义。方法:取健康雄性SD大鼠制备哮喘模型并诱发哮喘发作,采用中枢立体定位及微量注射技术,分3组分别在NTS内微量注射无菌生理盐水、H3受体激动剂R--αmethylhistamine(RMHA)以及H3受体拮抗剂thioperamide(Thio)加RMHA,用SABC免疫组织化学方法测定大鼠哮喘急性发作后1 h Fos蛋白在丘脑至延髓平面各核团的分布情况。结果:与哮喘组相比,哮喘大鼠NTS内微量注射1μg RMHA,丘脑室旁核、下丘脑室旁核、室周核、NTS等核团Fos蛋白表达减少,阳性细胞数降低,差异有显著性(P<0.01);而用Thio 5μg预处理则可拮抗RMHA的上述效应。结论:NTS内H3受体可能通过丘脑室旁核、下丘脑室旁核和室周核等脑区相关神经元参与对哮喘的神经调控,从而可能抑制哮喘发作。     

睡眠剥夺及恢复睡眠1小时后大鼠脑干中c—Fos蛋白的表达

目的：探讨睡眠剥夺和睡眠剥夺后恢复睡眠1小时后脑干中c-Fos蛋白的表达。方法：采用小平台水环境法建立大鼠睡眠剥夺模型,用Fos蛋白免疫组化的方法分别测量睡眠剥夺24小时组、睡眠剥夺24小时后恢复睡眠1小时组、大平台对照组、正常单独饲养组脑中Fos蛋白的表达,每组4只。结果：睡眠剥夺使Fos蛋白在脑干中不同区域的表达不同,主要区域有孤束核、臂旁核、脑桥被盖核、脑桥网状结构、蓝斑下核及被盖背外侧核;睡眠剥夺后1小时大鼠大部分时间在睡眠,并且上述区域Fos蛋白表达阳性程度减轻,为中低密度。结论：睡眠剥夺后1小时的恢复性睡眠可以使脑中c-Fos蛋白表达减轻。     

替加色罗对结肠炎诱导的大鼠腰骶髓Fos、P物质和降钙素基因相关肽表达的影响

背景:临床研究发现,替加色罗可以明显改善肠易激综合征患者的腹部不适和腹痛,但其调节内脏感觉的机制目前尚不清楚。目的:观察替加色罗对结肠炎诱导的大鼠腰骶髓Fos、P物质(SP)和降钙素基因相关肽(CGRP)表达的影响,探讨替加色罗降低内脏敏感性的作用途径。方法:成年雄性Sprague-Dawley大鼠24只,以三硝基苯磺酸灌肠诱导结肠炎并随机分为实验组1:替加色罗灌胃,每天2mg/kg;实验组2:替加色罗灌胃,每天1mg/kg;对照组:生理盐水灌胃,2.0ml/d。连续灌胃7天后,采用免疫组化方法检测大鼠腰骶髓Fos、SP和CGRP的表达。结果:结肠炎可诱导对照组大鼠腰骶髓(L5～S1)背角深层Fos表达以及背角浅层SP和CGRP表达。实验组1大鼠腰骶髓背角Fos阳性神经元数(22.0±7.7)和SP密度(12.5%±1.4%)显著低于对照组(62.2±18.9和35.9%±8.9%,P<0.05),CGRP密度(1.2%±1.1%)与对照组(2.8%±2.4%)相比无显著差异。实验组2大鼠腰骶髓背角Fos、SP和CGRP的表达与对照组相比均无显著差异。结论:替加色罗可以明显减少结肠炎诱导的大鼠腰骶髓背角Fos和SP的表达,其降低内脏敏感性的作用可能与抑制脊髓背角SP的表达有关。