氟中毒大鼠中缝背核5—羟色胺能神经元的免疫细胞化学研究

以饮用高氟水的方法制造了雄性大鼠慢性氟中毒模型。对脑干中缝背核５－羟色胺（５－ＨＴ）能神经元进行了免疫细胞化学定性、定量研究，结果显示，慢性氟中毒大鼠中缝背核５－ＨＴ能神经元略少，部分胞体缩小或肿大。胞质内５－ＨＴ阳性反应颗粒减少且界限不清。显微图像分析仪检测上述神经元内５－ＨＴ阳性反应颗粒明显减少。本研究揭示，高氟摄入对中枢５－ＨＴ能神经元有直接损害，对５－ＨＴ的产生有抑制作用。     

慢性氟中毒大鼠垂体生长激素细胞及下丘脑生长抑素神经元的免疫细胞化学研究

本实验对慢性氟中毒大鼠垂体生长激素(GH)细胞及下丘脑生长抑素(SS)神经元进行了免疫细胞化学染色,并用图像分析仪对GH及SS进行了半定量分析。结果表明:同对照组相比,氟中毒垂体GH细胞中的阳性反应颗粒细小并弥散地分布,半定量分析表明其GH含量明显低于对照组。未见下丘脑SS神经元及其SS含量有明显改变。本研究结果提示高氟可直接作用于垂体GH细胞影响其合成分泌功能。     

慢性氟中毒大鼠中缝核群5-羟色胺水平研究

氟中毒对中枢神经系统的影响日见关注[1]。已有研究表明,慢性氟中毒泌乳期大鼠下丘脑5-羟色胺(5-HT)水平降低[2];作者曾对慢性氟中毒哺乳期大鼠脑干中缝核群5-HT神经元形态结构及5-HT水平影响进行了免疫细胞化学研究[3]。但尚未见到慢性氟中毒大鼠中缝核群5-HT水平定量研究的报道。为此,本实验以饮用高氟水的方法复制了雄性大鼠慢性氟中毒模型,对脑干中缝核群5-HT水平进行定量研究,以便进一步探讨氟中毒对5-HT能神经系统的影响。1材料与方法1.1实验动物:取生后40日龄的Wistar系雄性大鼠16只,随机分为实验组和对照组各8只。实验组饮水…     

慢性氟中毒小白鼠哺育的仔鼠生长情况

以饮用高氟水的方法制造了雌性小白鼠慢性氟中毒模型。观察了氟中毒授乳小白鼠所哺育的仔鼠生长情况，以荧光分光光度法测定了氟中毒授乳小白鼠脑组织５－羟色胺（５－ＨＴ），５－羟吲哚乙酸（５－ＨＩＡＡ）和多巴胺（ＤＡ）的含量。结果不论仔鼠是否由对照组或实验组母鼠所生，只要其生后由对照组授乳鼠来哺育，则其体重增长情况正常；不论仔鼠是否由对照组或实验组所生，只要其生后由实验组授乳鼠来哺育，则其体重增长则显著落后     

慢性氟中毒大鼠垂体生长激素细胞及下丘脑生长抑素神经元…

本实验对慢性氟中毒大鼠垂体生长激素（ＧＨ）细胞及下丘脑生长抑素（ＳＳ）神经元分析了免疫细胞化学染色，并用图像分析仪对ＧＨ及ＳＳ进行了半定量分析，结果表明：同对照组相比，氟中毒垂体ＧＨ细胞中的阳性反应颗粒细小并弥散地分布，半定量分析表明其ＧＨ含量明显低于对照组，未见下丘脑ＳＳ神经元及其ＳＳ含量有明显改变，本研究结果提示高氟可直接作用于垂体ＧＨ细胞影响其合成分泌功能。     

慢性氟中毒大白鼠肝肾组织学观察

给大白鼠自饮含氟量为50ppm和75ppm的水100天,成功地建立了氟对软组织、特别是肝脏和肾脏发生病理改变的慢性氟中毒动物模型。     

慢性氟中毒大鼠大脑皮质NOS阳性神经元的变化

目的　探讨慢性氟中毒对大鼠大脑皮质一氧化氮合酶（NOS）阳性神经元的影响。方法　采用NADPH-黄递酶（NADPH-d）组织化学方法,标记大脑皮质NOS阳性神经元,对慢性氟中毒大鼠大脑皮质NOS阳性神经元变化进行计数。结果　慢性氟中毒大鼠皮质NOS阳性神经元数明显少于对照组（P<0.01）。结论　慢性氟中毒大鼠脑内皮质NOS阳性神经元的改变可能是氟中毒影响脑功能的重要原因之一。     

实验性氟中毒大鼠中缝背核神经元超微结构研究

以喂饲高氟（１００ｍｇ／Ｌ）水的方法制造了雄性大鼠慢性中毒模型，透射电子显微镜下观察了大鼠中缝背核（ＮＲＤ）神经元的超微结构变化。结果表明，氟中毒大鼠ＮＲＤ神经元出现超微结构改变。主要表现为神经元的核浆比值增大，核内异染色质增多且边集，线粒体扩张，嵴断裂或消失，粗面内质网池，高尔基复合体扁平囊亦扩张。神经元胞体，尤其是突起中脂褐素明显增多，并有较多的自噬体出现。个别神经元固缩。神经纤维有髓鞘松散及     

慢性氟中毒大鼠中缝大核硫胺素焦磷酸酶细胞化学研究

目的探讨慢性氟中毒对大鼠中缝大核酶活性的影响。方法饮用高氟水(100mg／L)复制雄性大鼠慢性氟中毒模型。对中缝大核神经元硫胺素焦磷酸酶(TPPase)进行定性、定量分析。结果氟中毒大鼠中缝大核神经元内TPPase染色浅于对照组，定量分析TPPase活性下降。电镜观察氟中毒大鼠神经元内TPPase颗粒减少，同时出现超微结构改变。结论高氟可抑制TPPase酶的活性，对中枢神经系统有直接损害作用。     

慢性氟中毒大鼠中缝大核超微结构的研究

目的：研究慢性氟中毒大鼠中缝大核的超微结构,方法：以饮用高氟水（100mg/L)的方法制造了雄性大鼠慢性氟中毒模型。透射电子显微镜下[观察了大鼠中缝大核的超微结构,结果：氟中毒大鼠中缝大核内的神经元出现超微结构改变,胞核内异染色质增多且边集,线粒体扩张,嵴断裂或消失,粗面内质网,高尔基复合体平囊亦扩张,胞体,尤其是突起中脂褐素明显增多,并出现较多的自噬体,个别神经元固缩,结论：高氟摄入对中缝大核神经元有直接损害作用。     

慢性氟中毒授乳大鼠垂体催乳素细胞的超微结构研究

在透射电镜下观察了慢性氟中毒授乳大鼠垂体前叶催乳素细胞的超微结构变化。按其改变程度可分为三种类型:其一,大多数催乳素(PRL)细胞的结构基本正带,只核的异染色质增多,大的成熟颗粒明显多于对照组;其二,有些 PRL 细胞内线粒体增多并明显肿胀,内嵴减少或破坏,高尔基复合体的大泡增多,胞质中有大脂滴沉积;其三,有少数 PRL 细胞退化变性。同时测定血清 PRL 水平降低,垂体 PRL 含量及浓度升高。以上结果提示:慢性氟中毒可能使催乳素的释放受阻,并且氟对 PRL 细胞可能有直接的毒性作用。     

Immunocytochemical localization of beta-endorphin-containing neurons in the rat brain

beta-Endorphin-containing neurons in the rat central nervous system were localized using three improvements of the unlabelled antibody-enzyme bridge immmunocytochemical technique. These improvements were (1) the use of brains from colchicine-treated rats; (2) the proteolytic pretreatment of sections with pronase, and (3) a 'double-bridge' staining procedure. In addition to the known localization of beta-endorphin-like immunoreactivity in perikarya in the medial basal hypothalamus, we have observed nerve fibers and terminals with beta-endorphin-like immunoreactivity to be more widely distributed than reported in previous studies. This includes discrete areas of the septal, preoptic, hypothalamic, thalamic and subthalamic regions, the amygdala, the periaqueductal gray, the inferior colliculus, the nucleus tegmenti pontis, the nucleus raphe dorsalis, several regions of the reticular formation, the locus ceruleus, the parabrachial nuclei, the mesencephalic trigeminal nucleus, the nucleus raphe magnus, the solitary tract and the nucleus of the solitary tract. The distribution of beta-endorphin-like immunoreactivity is in good agreement with many of the physiological, neuroendocrine and behavioral effects attributed to this peptide such as analgesia, the regulation of the release of pituitary hormones, thermoregulation and feeding behavior. This implicates beta-endorphin as an important neurotransmitter or modulator with specific functions within the central nervous system.     

Specific neurotoxin lesions of median raphe serotonergic neurons disrupt maternal behavior in the lactating rat

Impairments in lactation after electrolytic lesions of the median raphe (MR) nucleus have been corrected by treatment with PRL. Specific serotonin neurotoxin lesions were used in the present study to determine whether decrements in litter growth after electrolytic lesions could be attributed to serotonergic neuron damage at the MR locus, and whether MR lesions (MRL) disrupted suckling-induced PRL release. Intracerebral microinjection of 5,7-dihydroxytryptamine (5,7-DHT) into the MR nucleus produced dose-related decrements in litter growth after either 4 micrograms (sham, 1.35 +/- 0.05; MRL, 1.04 +/- 0.05 g/pup X day; P less than 0.001) or 8 micrograms 5,7-DHT (sham, 1.35 +/- 0.06; MRL, 0.87 +/- 0.11 g/pup X day; P less than 0.001). Despite hypothalamic serotonin depletions of 15% and 55%, respectively, for the two doses of 5,7-DHT, there was no difference between sham and MRL animals in either basal or suckling-induced PRL release. When lesions were placed on day 1 of lactation (L) so that killing on day 7-L corresponded to the early maximal neurotoxin effect, MRL mothers still showed litter growth decrements (0.37 +/- 0.07; sham, 0.98 +/- 0.08 g/pup X day; P less than 0.001) and normal PRL values. When maternal behavior was examined, MRL animals exhibited a higher incidence of abnormal behaviors (failure to retrieve pups, cannibalism, and failure to initiate suckling during a 1-h test period; Fisher's exact P, Sham vs. MRL, less than 0.01, less than 0.05, and 0.15, respectively) than sham animals or animals with 5,7-DHT lesions in the dorsal raphe nucleus or superior colliculus. In addition, suckling behavior scores, determined from daily suckling behavior observations, were lowest in the MRL group and correlated with litter growth only in this group (r = 0.789; P less than 0.01). These data suggest that serotonergic elements in the MR nucleus play an obligatory role in maintaining normal maternal behavior during lactation, but they are not involved in suckling induced PRL release.     

Expression of endonuclease G in the brain tissue of rats with chronic fluorosis

正Objective To investigate the possible mechanism of endonuclease G(Endo G)-mediated non-Gaspase-dependent apoptotic pathway in brain neuronal apoptosis in chronic fluorosis rats.Methods Sixty Sprague Dawley(SD)rats(half male and half female)were randomly divided into two groups:control group fed with tap water with fluoride content0.05 mg/L and fluorine group in which sodium fluoride was added into drinking water with     

燃煤型氟中毒对大鼠中脑黑质神经元的影响

目的观察燃煤型氟中毒大鼠中脑黑质神经元的形态学变化,为地方性氟中毒引起脑损伤的发病机制提供实验依据。方法取SPF级SD大鼠90只,随机分为正常对照组、低氟组（3.3 mg/kg）和高氟组（106 mg/kg）,每组30只,雌雄各半。除对照组食用正常饲料外,其他各组均食用不同配方饲料,复制氟中毒大鼠模型。6个月后采用比色法测定各组大鼠黑质胆碱酯酶活性,然后取中脑黑质进行尼氏染色,TUNEL法细胞凋亡染色及TH免疫组化染色,光镜观察3组大鼠黑质神经元的形态变化,并测量TH阳性反应产物的平均光密度。结果随着染毒剂量的增加主要有：尿氟含量逐渐增多（P〈0.05）;学习记忆能力与胆碱酯酶活性逐渐下降（P〈0.05）;黑质细胞凋亡数量增多（P〈0.05）,TH阳性神经元减少（P〈0.05）。结论燃煤型氟中毒大鼠随染毒剂量的增加中脑黑质TH阳性神经元减少,细胞凋亡数量增多,这些变化可能是氟的神经毒性作用之一。     

Data supporting a new physiological role for brain apelin in the regulation of hypothalamic oxytocin neurons in lactating rats

Apelin is a bioactive peptide identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ in 1998. The present data show that apelin modulates the activity of magnocellular and parvocellular oxytocin (OXY) neurons in the lactating rat. A combination of in situ hybridization and immunohistochemistry demonstrated the presence of apelin receptor mRNA in hypothalamic OXY neurons. Double immunofluorescence labeling then revealed the colocalization of apelin with OXY in about 20% of the hypothalamic OXY-positive neurons. Intracerebroventricular apelin administration inhibited the activity of magnocellular and parvocellular OXY neurons, as shown by measuring the c-fos expression in OXY neurons or by direct electrophysiological measurements of the electrical activity of these neurons. This effect was correlated with a decrease in the amount of milk ejected. Thus, apelin inhibits the activity of OXY neurons through a direct action on apelin receptors expressed by these neurons in an autocrine and paracrine manner. In conclusion, these findings highlight the inhibitory role of apelin as an autocrine/paracrine peptide acting on OXY neurons during breastfeeding.     

Neural mechanisms of swallowing: Neurophysiological and neurochemical studies on brain stem neurons in the solitary tract region

Neurophysiological studies of the nuclei of the tractus solitarius (NTS) and adjacent regions have provided a partial understanding of the integrative brainstem network underlying swallowing and related functions such as respiration. The NTS is also richly endowed with an abundance of neuropeptides and other neuroactive substances, but only limited information is available on their influences on neurons involved specifically in swallowing. Since dysfunction of these neurophysiological and neurochemical regulatory mechanisms in the NTS region may be important in pathophysiological conditions such as dysphagia, increased awareness of and focus on these mechanisms are warranted. This paper outlines recent neurophysiological and neurochemical data that provide information on the afferent inputs and neurophysiological properties of neurons in NTS and adjacent caudal brainstem regions implicated in swallowing, respiration, and respiratory-related reflexes.