雌激素受体α在雌性大鼠脑中的表达

本试验利用免疫组织化学SP法,研究了雌激素受体α在大鼠脑中的表达.结果表明,ER_α免疫反应产物主要定位于神经元细胞核,部分区域出现阳性神经元和阳性突起,在海马CA1、CA2辐射层、齿状回、下托的分子层等出现阳性星形胶质细胞;ER_α在脑中表达广泛,免疫反应产物在端脑的隔外侧核、海马锥体细胞层、大脑皮质等,间脑的缰内侧核、下丘脑室旁核、弓状核、视上核等,中脑的动眼神经核,脑桥的脑桥核外侧部等为高密度;在端脑的尾壳核、杏仁中央核、海马CA4区,间脑的下丘脑室周核、缰外侧核等,中脑的黑质致密带,脑桥的脑桥被盖核等为较高密度;在问脑的视前室周核、丘脑后核、中脑的红核、脑桥的脑桥被盖网状核等为中等密度;在端脑的苍白球,间脑的无名质,无免疫反应产物出现.结果显示,雌激素在调节脑的认知和生殖内分泌过程中,ER_α可能起主要作用;雌激素可通过ER_α调节星形胶质细胞功能.     

乌鸡小脑的解剖学及神经肽Y神经元分布的研究

为了探明乌鸡小脑的形态结构及其细胞构筑和神经肽Y免疫反应神经元在小脑内的分布情况 ,采用石蜡切片HE染色和免疫组化SABC染色技术 ,对 1 0只泰和乌鸡的小脑进行了研究 ,并与北京鸭、肉鸽、本地鸡及非洲鸵鸟等禽类的相关结构进行了比较。结果表明 :①泰和乌鸡小脑皮质分 3层 ,由外至内依次为分子层、蒲肯野氏细胞层和颗粒层 ;②小脑分 1 0叶 ,Ⅰ、Ⅱ和Ⅹ为单叶 ,其余都有2个～ 3个小叶 ;③小脑中央核的神经元数量稀少 ;④神经肽Y免疫阳性神经元主要存在小脑皮质的蒲肯野氏细胞层 ,分子层、颗粒层 ,在小脑中央核未见阳性反应细胞 ;⑤泰和乌鸡小脑的形态结构及其细胞构筑与其它家禽相似 ;⑥小脑内NPY阳性神经元在蒲肯野氏细胞层的分布与鸡、肉鸽、大鼠的大体相似 ,在小脑白质内与肉鸽的有一定差异     

Ghrelin免疫反应阳性神经元在鸡脑中的定位分布、发育性变化及禁食对其影响

本试验应用免疫组织化学方法和显微图像分析技术,研究了鸡脑Ghrelin免疫反应阳性神经元的定位分布,分析了2、16、30、44、58日龄鸡下丘脑Ghrelin免疫反应阳性神经元的发育性变化规律,并探讨了30日龄鸡分别禁食12、24、48h及重新采食4h对下丘脑Ghrelin免疫反应阳性神经元的影响。结果表明,在下丘脑弓状核、室旁核、内侧核、室周区、内侧区、外侧区,丘脑卵圆核、圆核,中脑丘中央灰质层、红核,脑桥前庭腹外侧核,小脑内侧核、小脑皮质颗粒层,大脑皮质多形细胞层等,均可观察到Ghrelin免疫反应阳性神经元;随着日龄的增长,下丘脑主要核团中的Ghrelin免疫反应阳性神经元的数量增多,免疫反应强度增强,但细胞密度下降;在禁食条件下,下丘脑Ghrelin免疫反应阳性神经元的免疫反应强度减弱,细胞密度下降。     

鸡小脑突触素的表达与发育研究

应用免疫组织化学SP法，研究了突触素在15、20胚龄、10日龄鸡小脑中的表达。结果表明：突触素免疫反应产物以颗粒、小点、阳性神经元和阳性纤维形式出现；突触素免疫反应产物密度在15、20胚龄、10日龄有3种变化趋势：①分子层、颗粒层、中间核、外侧上核、外侧下核中随胚(日)龄增加保持不变；②蒲肯野氏层随胚(日)龄增加先升高后降低；③小脑内侧核则随胚(日)龄增加逐渐升高。结果揭示：突触素最终合成部位可能在高尔基复合体；20胚龄左右是蒲肯野氏层突触形成的高峰期；小脑各部突触在出壳前后发育具有不均衡性。     

强啡肽A_（1－13）免疫反应神经元在鸡脑的定位──ABC法研究

取健康成鸡（星杂２８８）１０只，经秋水仙素处理，灌流固定后取脑，作冰冻连续切片，ＡＢＣ法显示，鸡脑强啡肽Ａ１－１３（ＤｙｎＡ１－１３）免疫反应神经元分布于端脑的上纹状体、新纹状体、旧纹状体、外纹状体、海马、旁嗅区和伏隔核；间脑的下丘脑外侧核、丘脑背内侧核后部、丘脑背外侧核后部、室旁核和视前大细胞核等；中脑和延髓的视峡核、中脑外侧核背侧部、峡核、视叶脑室室周灰质、螺旋外侧核、被盖背外侧核、三叉神经中脑核、动眼神经核、中脑中央灰质、前庭核和延髓背侧网状核等。在侧脑室、第三脑室、中脑导水管和视叶脑室的室管膜上有阳性细胞和纤维分布，与脑脊液接触。结果表明，鸡脑ＤｙｎＡ１－１３阳性神经元分布十分广泛，提示ＤｙｎＡ１－１３可通过侧脑室、第三脑室、中脑导水管和视叶脑室释放入脑脊液。     

神经肽Y免疫反应神经元在鸽小脑中的定位--SABC 法研究

采用石蜡切片和免疫组化SABC法（链霉亲合素-生物素-过氧化物酶连结法），对10只肉鸽小脑内神经肽Y免疫反应神经元的分布状况进行了研究．并与北京鸭、鸟鸡、肉鸡及大鼠的相关结果进行了比较。在光镜下观察分析了阳性神经元的分布状况．并用图像分析软件进行了半定量分析。结果显示：（1）小脑内神经肽Y（neuropeptide Y，NPY）阳性神经元主要存在于小脑皮质的蒲肯野氏细胞层，且以小叶顶端的蒲肯野氏细胞阳性明显；（2）小脑白质中央核可见到少量阳性神经元．不同于鸟鸡、肉鸡及大鼠；（3）分子层、颗粒层未见阳性反应细胞。表明：鸽小脑NPY阳性神经元的分布在皮质中与鸡、大鼠大体相似；在白质中与鸡、大鼠有差异。     

鸡端脑和下丘脑向面神经腹侧核的传出性纤维联系—HRP逆行追踪法

将２０％ＨＲＰ水溶液注射于鸡的面神经腹侧核，逆行追踪支配该部的有关主同位神经核团。结果于端，下丘脑和脑干内出现标记细胞，端脑内的标记细胞较多地出现于古纹状体，少量出现于旧纹状体腹侧与枕中脑束之间的区域，两群标记细胞形态上明显不同。下丘脑的标记细胞较多地出现于下丘脑后区，室旁核出现少量，个别散在于下丘脑其他区域。     

强啡肽A1—13免疫反应神经元在鸡脑的定位：ABC法研究

取健康成鸡（星杂２８８）１０只，经秋水仙素处理，灌流固定后取脑，作冰冻连续切片，ＡＢＣ法显示，鸡脑强啡肽Ａ１－１３（ＤｙｎＡ１－１３）免疫反应神经元分布于端脑的上纹状体，新纹状体、旧纹状体、外纹状体、海马、旁嗅区和伏隔核；间脑的下丘脑外侧核、丘脑背内侧核后部、丘脑背外侧核后部，室旁核和视前大细胞核等；中脑和延髓的视峡核，中脑外侧核背侧部、峡核、视叶脑室室周灰质、螺旋外侧核、被盖背外侧核、三叉神经中     

鸡端脑向小脑投射的起始核

将40%辣根过氧化物酶（HRP）水溶液注入鸡小脑的Ⅵ、Ⅶ、Ⅷ叶，逆行追踪其端脑向小脑投射的起始核。结果发现，端脑的海马列、隔核、带核、旁嗅叶出现多量标记细胞；副高纹状体、嗅结节和古纹状体出现少量标记细胞。将CB-HRP引入古纹状体，于小脑皮层的分子层内出现顺行标记物，颗粒层内也有稀疏的顺行标记物出现。结果表明，鸡端脑-小脑投射的起源较为丰富而广泛，上世纪初提出的纹-小脑束可能起始于古纹状和带核。     

雌激素对去卵巢大鼠小脑ER、ChAT、NGF表达的影响

本研究旨在探讨雌激素对大鼠小脑内雌激素受体（ER）、神经生长因子（NGF）和胆碱乙酰转移酶（ChAT）表达的影响。建立去卵巢SD大鼠模型,以小脑为研究对象,运用免疫组织化学SP法,通过补充17β-雌二醇对ER、NGF和ChAT在小脑中的表达和分布变化进行研究。结果表明：ER、NGF和ChAT免疫阳性反应物在小脑皮质主要分布于蒲肯野氏细胞,而在小脑核中主要定位于小脑顶核、间位核和齿状核;ER阳性产物主要定位于细胞质和突起中,也存在于胞膜和胞核中。去卵巢大鼠小脑中3种阳性物质的表达强度及阳性细胞数量总体呈显著降低趋势,在补充17β-雌二醇后,3种阳性物质的表达强度和阳性细胞数目显著回升。本试验证实雌激素可促进小脑中NGF和ChAT的表达;另外ER、NGF和ChAT表达变化的相似性提示三者在雌激素对小脑的作用中是相互调节和影响的,同时表明雌激素可能既通过基因组机制,也通过非基因组机制途径在小脑发挥作用。     

Morpho- und Histogenese der Colliculi rostrales beim Rind

Based upon macroscopic and light microscopic examinations the development of the superior colliculus of bovine embryos and fetuses with crown-rump lengths (CRL) ranging from 0.8 to 90.0 cm was studied. Macroscopically, the mesencephalon can be recognized for the first time at 0.8 cm CRL, whereas the superior colliculus can be clearly differentiated in embryos of 4.5 cm CRL. The macroscopic features of this brain area have reached adult conditions at 80.0 cm CRL. The light microscopic examination reflected the beginning of layer formation at 0.8 cm CRL, which is induced by the proliferating activity of the ventricular zone. Up to 3.4 cm CRL the primordium of the tectum opticum exhibits still a trilaminate pattern (ventricular-, intermediate- and marginal zone), but at 4.5 cm CRL, the formation of the specific tectal layers is marked by the origin of the stratum profundum and intermedium. With the appearance of the tenth layer named stratum opticum at 8.0 cm CRL the laminar pattern corresponds to the characteristics of adult animals.     

Cerebellar cortical abiotrophy in Lagotto Romagnolo dogs

This case report documents two pathological variations of potentially inherited, cerebellar cortical abiotrophy in two unrelated Lagotto Romagnolo breed dogs. The first dog had an atypical lesion in the cerebellar cortex with depletion of cerebellar granular cell layer and sparing of the Purkinje cell layer. The second case had degenerative changes in both Purkinje and granular cell layers. The clinical picture was similar in both cases presented, although the severity of the signs of cerebellar dysfunction varied.     

Neuronal apoptosis in the developing cerebellum

The following study analysed apoptosis in proliferative cells and migrating neurons of the developing cerebellum. The external granular layer, Purkinje cell layer and internal granular layer in the developing mouse cerebellar cortex were analysed by active caspase-3 immunohistochemistry, Hoechst 33258 staining and Western blot analysis. Immunocytochemistry results indicated that the peak of apoptosis appeared at postnatal days P8, P5 and P9 in the external granular layer, Purkinje cell layer and internal granular layer, respectively. Subsequently, in each region, the rate of apoptosis decreased with increasing age. In contrast, Western blot results demonstrated the highest expression of activated caspase-3 in the cerebellum at P5, followed by a subsequent decline and disappearance of expression by P14. Activated caspase-8 was expressed maximally at P10, and subsequently disappeared by P30. The results of this study suggest that the key period of neuronal apoptosis in the cerebellar cortex is between P0 and P14, indicating that this developmental period could be susceptible to treatment for congenital neurodegenerative diseases.     

Afferent and efferent connections of the nucleus geniculatus lateralis ventralis demonstrated by WGA-HRP in the chick

Fibre connections of the chick nucleus geniculatus lateralis ventralis (GLv) were investigated using the axonal tracing method with wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). After an injection of WGA-HRP into the GLv, many labelled neurons were observed in layer i of the stratum griseum et fibrosum superficiale (SGFS) in the ipsilateral tectum opticum (TO) and in the nucleus lentiformis mesencephali (LM). In the TO-GLv projection, cells of origin were located in the deeper part of layer i of the TO and were topographically distributed along the direction from the rostrodorsal part to the caudoventral part of the TO relating to a rostrocaudal axis of the GLv. In the LM-GLv connection, the dorsal and ventral parts of the LM connected reciprocally with the rostral and caudal halves of the GLv, respectively. In contrast, in the GLv efferent connection, labelled axon terminals spread widely in the ipsilateral area pretectalis without any clear topographical arrangement.     

Hereditary cerebellar degenerative disease (cerebellar cortical abiotrophy) in rabbits

A pair of rabbits gave birth to a set of littermates (F1) with symptoms of early-onset ataxia. Microscopic examination revealed cerebellar degenerative disease in 5 of 6 littermates. Light microscopy was used to compare the thickness of each cerebellar layer in affected animals in contrast to a normal control. Affected animals showed narrowing of the molecular layer of the vermis, reduced density of Purkinje cell dendrites and irregular thickness in their branchlets, and reduced density of granular cells and scattered pyknotic cells in the granular layer. Pyknotic cells were apoptotic granular cells, confirmed by positive staining using the TUNEL method. Electron microscopy confirmed the thinning of the molecular layer seen by light microscopy and also showed a reduced number of parallel fibers, which indicate granular cells axons, and a reduced number of synaptic junctions between Purkinje and granular cells. Purkinje cells had electron-dense, irregularly shaped cytoplasm with irregularly shaped nuclei, and some of these cells had a central chromatolysis-like region. These findings support a diagnosis of cerebellar cortical abiotrophy, a hereditary condition that causes nerve function impairment leading to early-onset progressive degeneration of the cerebellar cortex.     

Distribution of Prosaposin mRNA in the Central Nervous System of the Pigeon (Columba livia)

Bioassay and immunohistochemical studies have detected the presence of prosaposin in the central nervous system (CNS) of mammals. Here, first time, we have determined the partial cDNA sequence of pigeon prosaposin and mapped the distribution of its mRNA in the pigeon CNS. The predicted amino acid sequence of pigeon prosaposin showed 93 and 60% identity to chicken and human prosaposin, respectively. In situ hybridization, autoradiograms showed that the prosaposin mRNA expression was found in the olfactory bulb, prepiriform cortex, Wulst, mesopallium, nidopallium, hippocampal formation, thalamus, tuberis nucleus, pre‐tectal nucleus, nucleus mesencephalicus lateralis, pars dorsalis, nucleus isthmi, pars parvocellularis and magnocellularis, Edinger–Westphal nucleus, optic tectum, cerebellar cortex and nuclei, vestibular nuclei and gray matter of the spinal cord. These results suggest that the cDNA sequence of pigeon prosaposin is comparable to other vertebrates, and the general distribution pattern of prosaposin mRNA resembles those are found in mammals.     

Cerebellar hypoplasia associated with an avian leukosis virus inducing fowl glioma

Fowl glioma-inducing virus (FGV), which belongs to subgroup A of avian leukosis virus (ALV), shows tumorigenicity and pathogenicity, mainly in the nervous system, and causes astrocytoma and perineurioma. Apart from these neoplasms, cerebellar anomaly was found in chickens infected with FGV in ovo. The study reported here describes the morphologic characteristics of the affected cerebellum. Specific-pathogen-free chickens (C/O) were inoculated with FGV through the yolk sac on the 7th day of incubation. The cerebellar anomaly included diffuse depletion of granular cells of the internal granular layer (IGL), remnants of the external granular layer (EGL), and disorganization of the Purkinje cell layer. These cerebellar changes were observed in all birds except one. In the infected embryos, the EGL was thicker and had an irregular arrangement with a thin molecular layer (ML) and IGL, compared with the control. The granular cells were immunohistochemically positive for ALV common antigen. Immunohistochemical analysis for vimentin revealed disarrangement and decreased number of Bergmann's fibers. Use of the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method and electron microscopy indicated that apoptotic granular cells were frequently observed in the EGL and ML. These results suggested that the cerebellar anomaly was hypoplasia, principally resulting from the apoptosis of granular cells in the EGL and ML caused by FGV infection and that the cell loss induced obstruction of granular cell migration and disarrangement of Bergmann's fibers in the ML.     

Cerebellar cortical abiotrophy in American Staffordshire terriers: clinical and pathological description of 3 cases

Three American Staffordshire Terriers were presented with gait abnormalities and loss of balance at the age of 4.5 (female) and 6 years (2 males). The onset varied between 3 and 5 years of age and the clinical signs were slowly progressive. The neurological examination revealed symmetrical generalized cerebellar ataxia with hypermetria, stiffness, and loss of balance with no evidence of paresis. The menace reflex was decreased in one dog and absent in another. A positional nystagmus was found in two dogs. The dogs were euthanized and a histopathological examination of each brain was performed. Pathological changes were confined to the cerebellum. The main finding was loss of Purkinje cells, as well as depletion of granular cell bodies and shrinkage of the granular and molecular cell layer. These findings are consistent with cerebellar cortical abiotrophy. A genetic basis is supposed, but the mode of inheritance is not determined yet. In contrast to some spinocerebellar ataxias in humans, the cause of Purkinje cell degeneration in cerebellar cortical abiotrophy of dogs is not known.