大鼠下丘脑弓状核神经元的衰老性变化

选用青、中年和老年雄性大鼠各１０只，用形态计量学和体视学方法定量分析弓状核神经元年龄性变化。结果发现在老年大鼠弓状核，部分暗型和亮型神经元内粗面内质网排列紊乱、缩短和双层膜间隔增宽，线粒体嵴断裂、肿胀和空泡化，溶酶体，微管和颗粒小泡数减少；与青、中年组比较神经元数分别丢失３７％和２７％，核仁平均体积缩小３０％左右；     

高脂血症对大鼠大脑皮质神经肽Y能神经元的影响

目的观察高脂血症对大鼠大脑皮质神经肽Y(neuropeptide Y,NPY)能神经元的影响。方法雄性SD大鼠60只,随机分为实验组和对照组(n=30)。实验组饲以高脂饲料,于高脂饲料喂养7d、30d、90d后取大脑组织行免疫组化染色,显微图像分析。结果与正常对照组相比,高脂饲料喂养30d和90d后,大鼠血清总胆固醇浓度显著升高,NPY免疫阳性神经元数目和光密度增加(p<0.05),90d显著增加(p<0.01)。结论高脂血症时,NPY在大鼠大脑皮质过表达。     

大鼠下丘脑弓状核神经元的神经支配

用ＨＲＰ逆行追踪和免疫细胞化学与电镜结合法研究了下丘脑弓状核神经元的神经支配。结果表明，室旁核向弓状核投射的神经元中，有一部分为催产素免疫反应阳性，一部分为后叶加压素免疫反应阳性，视上核也有部分ＯＴ免疫反应阳性神经元发出纤维投射至弓状核。将零乱毒素Ｂ亚单位结合ＨＲＰ注入第三脑室后，可见弓状核内有逆行标记细胞，电镜观察发现弓状核内的脑啡肽免疫反应阳性的树突接受ＨＲＰ反应阳性的触液神经元的轴突形成突触     

动脉粥样硬化大鼠弓状核和视前内侧区神经元的形态变化

用雄性大鼠６只，一次性腹腔注射ＶＤ６０万单位／ｋｇ体系，存活３５天后，取下丘脑作石蜡连续切片，用体视学方法分析了下丘脑弓状核和视前内侧区神经元的参数变化。结果发现：下丘脑区两相核团的神经元体积变小，数目增多，发生了明显的形态学改变。     

老年大鼠下丘脑视上核和弓状核的超微结构变化

观察老年大鼠下丘脑视上核腹侧大细胞神经元和弓状核神经元的超微结构,结果显示:老年大鼠视上核腹侧血管加压素(VP)神经元的胞体较成年鼠大,胞质结构比较致密,内含许多核糖体颗粒,粗面内质网分散成小泡状,神经分泌颗粒增多,溶酶体、线粒体、高尔基氏复合体数量都较多.而弓状核内的暗细胞和亮细胞的核糖体减少,高尔基氏复合体和线粒体都变化,还有少数神经元固缩,细胞质内胞器明显减少,呈现变性现象.结果提示:老年期下丘脑视上核VP神经元机能增强;而弓状核内两种细胞都显示机能减弱的征象.老年时下丘脑各核团神经元的这种不协调性变化,可能是动物衰老的一种重要表现.     

谷氨酸单钠对新生期大鼠弓状核神经元毁损的实验研究

目的;探讨谷氨酸单钠对新生期大鼠弓状核神经元的损伤作用。方法：将初生Ｗｉｓｔａｒ仔鼠１２只于第１、３、５、７、９天皮下注射１０％谷氨酸单钠４ｇ／ｋｇ体重,分别存活５与１０周;对照组的新生期鼠同时注射等量生理盐水,成年鼠注射谷氨酸单钠存活１０周。取下丘脑固定,作甲苯胺兰染色,光镜观察。结果：谷氨酸单钠可选择性地毁损新生期鼠下丘脑弓状核神经元,１０周组在核内神经细胞几乎消亡,残存的细胞不超过１０％。而     

高脂血症大鼠大脑中动脉神经肽Y能神经纤维的变化

观察高脂血症大鼠不同时期大脑中动脉神经肽Ｙ能神经纤维的变化。方法ＡＢＣ免疫组人方法；结果（１）定性观察；对照组各时期神经肽育神经纤维多呈网状攀附于血管周围，纤维较稀疏，并有明显的串珠状膨体；高脂组纤维亦呈网状分布于血管周围，较稠密，膨体清晰可见，这种变化见一实验组各时期。     

弓状核内神经紧张素能神经元与神经肤Y能神经元关系的免疫电镜双标记研究

用包埋前免疫电镜PAP双标记技术,对大鼠下丘脑弓状核内的神经紧张素(NT)和神经肽Y(NPY)的分布进行了超微结构研究。先用DAB法显示NPY免疫反应。然后用钼酸铵-TMB法显示NT免疫反应,再经DAB-氯化钴稳定后作免疫电镜包埋。结果:在弓状核内,NPY免疫反应产物呈电子密度高的颗粒状或絮状沉淀,弥漫分布于核周质的细胞器和基质、树突的微管周围、轴突的小透亮囊泡周围。NT免疫反应产物则为致密的针状或块状,散在分布于核周质、树突和轴突内。两者极易分辨。NPY能和NT能神经结构在弓状核内呈交错分布,彼此关系密切。含NPY的树突和轴突与免疫反应阴性轴突形成突触连接;含NT的胞体和树突与免疫反应阴性轴突形成突触连接。此外,NPY阳性轴突末梢还与NT阳性树突形成对称性轴-树突触。本研究结果为下丘脑NT能神经元的肽能突触调节提供了又一新的超微结构依据。     

不同时程应激对大鼠下丘脑弓状核和室周核神经细胞的影响

目的:观察不同时程应激对大鼠下丘脑弓状核和室周核神经细胞的影响及酪氨酸羟化酶(TH)的表达变化,为应激性损伤的机制研究提供病理形态学依据。方法:建立每日束缚固定8 h加冰水游泳5 min的应激大鼠模型,分为1、3、7、14、21d组及各时间点正常对照组,采用硫堇染色观察弓状核、室周核内神经细胞尼氏体变化及细胞形态学改变;TH免疫组织化学标记观察大鼠下丘脑弓状核和室周核内多巴胺能神经细胞阳性表达变化,采用全景组织细胞定量分析系统,进行统计分析。结果:较长时程反复的应激刺激导致了大鼠弓状核和室周核神经细胞细胞质内尼氏体消失及部分细胞固缩。TH免疫组织化学标记显示随着应激时程的延长,下丘脑弓状核和室周核内多巴胺能神经细胞阳性表达数目减少。结论:较长时程的反复应激刺激可导致大鼠下丘脑弓状核和室周核神经细胞损伤及多巴胺能神经细胞缺失。     

Coexistence of neuropeptide Y and somatostatin in rat and human cortical and rat hypothalamic neurons

The distribution and coexistence of neuropeptide Y (NPY) and somatostatin (SOM) were evaluated in rat and human cerebral cortex and in the rat hypothalamic arcuate nucleus (n) using double immunofluorescent staining in which primary antisera were raised in different species. The results of the study indicate extensive coexistence of NPY and SOM in both rat and human cortex but only occasional coexistence in the rat arcuate n.     

PACAP deficient mice display reduced carbohydrate intake and PACAP activates NPY-containing neurons in the rat hypothalamic arcuate nucleus

Pituitary adenylate cyclase-activating polypeptide (PACAP) potentiates both insulin release from islets and insulin action in adipocytes. Therefore, this peptide is considered a regulator of glucose homeostasis. PACAP and its receptors are localized not only in the peripheral tissues but in the central nervous system. The present study examined whether PACAP regulates the feeding behavior and the activity of neurons in the hypothalamic arcuate nucleus (ARC), a feeding center. Food intake was measured in the PACAP knock-out mice. Cytosolic Ca²⁺ concentration ([Ca²⁺]_i) in single neurons isolated from the ARC of rats was measured by fura-2 microfluorometry, followed by immunocytochemical staining with anti-NPY antiserum. PACAP knock-out mice showed a decrease in the intake of high carbohydrate, but not high fat, food. PACAP increased [Ca²⁺]_i in NPY neurons of the ARC that are implicated in the feeding, particularly the carbohydrate ingestion. Agonists of PACAP receptors, PAC1-R and VPAC2-R, also increased [Ca²⁺]_i. The present study, by demonstrating that PACAP directly reacts with the ARC NPY neurons to increase [Ca²⁺]_i and that ingestion of the carbohydrate-rich food is reduced in PACAP-deficiency, suggests a facilitative role for PACAP in the carbohydrate intake.     

Demonstration of gastrin/cholecystokinin-like immunoreactivity in the arcuate nucleus, median eminence and pituitary of the guinea pig

In the brains of colchicine-treated guinea pigs, antibodies directed against the C-terminal sequence of cholecystokinin octapeptide (CCK-8) and cross-reacting with gastrin, visualized a dense population of cell bodies in the arcuate nucleus, periportal nerve endings in the external layer of the median eminence and a few fibers in the neurohypophysis. In the adenohypophysis, at least the major part of corticomelanotrophs were labelled. Immunostainings are compared to those reported in the rat.     

Tachykinin-induced changes in β-endorphin gene expression in the rat arcuate nucleus

Previous neuroanatomical data have indicated the presence of synaptic connections between tachykinergic terminals and proopiomelanocortin (POMC) neurons in the arcuate nucleus. Consequently, tachykinins may regulate the activity of POMC neurons. To evaluate the functional signification of this regulation, the effect of intracerebroventricular injections of neurokinin A (NKA) on POMC mRNA levels was studied by using in situ hybridization. Repeated injection of NKA (40 μg/animal per day during 3 days) induced a 48% increase in POMC mRNA expression as compared to NaCl injected control animals. In conclusion the results of this study show an excitatory effect of tachykinin on POMC neurons and suggest a direct and/or indirect excitatory control of POMC neuronal activity by endogenous tachykinins.     

Cytometric investigations in histochemically identified neurons — Changes of fluorescence intensities and nuclear diameters in dopamine neurons of the arcuate nucleus in the cycling rat

Summary The relative formaldehyde-induced fluorescence intensities and the diameter of cell nuclei of fluorescent perikarya of the arcuate nucleus were recorded in serial cross-sectioned hypothalamic arcuate nuclei of regularly cycling rats (5 estrous and 4 proestrous animals). Stress-induced changes of cytometric parameters were avoided by preadaptation of animals to handling procedures. Dopamine neurons in a 75 m thick periventricular layer of the arcuate nucleus exhibited significantly smaller nerve cell nuclei and significantly reduced relative fluorescence intensities in proestrous rats. Both of these cytometric parameters indicate a decrease in the activity of periventricular dopamine neurons of the arcuate nucleus. The reported findings might support the hypothesis that dopamine inhibits the release of LH-RH.In partial fulfillment of requirements for an academic degree (Dr. med.)Supported by a grant from the Deutsche Forschungsgemeinschaft (-Ha 726/5-) and the Stiftung Volkswagenwerk (I/35 582) to H.G.H.     

Synaptic relationships between induced neuropeptide Y-like immunoreactive terminals and cuneothalamic projection neurons in the rat cuneate nucleus following median nerve transection

Previous studies have demonstrated that following complete median nerve transection (CMNT), neuropeptide Y-like immunoreactive (NPY-LI) fibers were dramatically increased and predominantly expressed in the ventral portion of the middle cuneate nucleus (CN), reaching maximum numbers at four weeks. Ultrastructurally, NPY-LI terminals made axodendritic synapses, but the postsynaptic elements are unknown. In the present study, using retrograde tract-tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) and NPY immunocytochemistry we examined the synaptic relationships between cuneothalamic projection neurons (CTNs) and NPY-LI terminals in the rat CN following CMNT. The injury-induced NPY-LI fibers were distributed throughout the rostrocaudal extent of the CN. Further, the greatest number of HRP-labeled CTNs was observed in the ventral portion of the middle CN. Ultrastructurally, the NPY-LI terminals made asymmetric axodendritic synaptic contact with the HRP-labeling CTN dendrites. These data suggest that injury-induced NPY may modulate the excitability of CTNs, and thus, play a role in the transmission of neuropathic sensation following median nerve injury.     

Morphological evidence for synaptic junctions between substance P-containing neurons in the arcuate nucleus of the rat

The presence of synaptic junctions between substance P-containing neurons (SP neurons) was shown in the hypothalamic arcuate nucleus of rats by pre-embedding electron microscopic immunohistochemistry. The immunoreactive perikarya were synapsed by immunoreactive fiber terminals as well as immunonegative fiber terminals. The functional implication of the synapses between SP neurons is discussed in relation to autoregulatory mechanisms of the neurons.