牦牛大脑皮层厚度及神经元密度的增龄性变化

为探究高原牦牛低氧适应过程中,大脑皮质厚度及其神经元密度的增龄性变化及规律,试验应用组织学技术及图像分析软件分别测量不同发育期(1日龄、30日龄、180日龄和成年)高原牦牛枕叶、额叶、顶叶、颞叶的皮质厚度及神经元密度,并对试验数据进行单因素方差分析。结果表明:牦牛枕叶、额叶、顶叶的皮质层总厚度随年龄增长而增厚(P0.05),颞叶皮质层总厚度在成年时略有减小(P0.05),但整体为随年龄增长而增厚(P0.05)。30日龄时,枕叶外锥体层、内颗粒层及内锥体层厚度,顶叶外锥体层厚度及颞叶内颗粒层厚度处于较低水平;180日龄时,额叶外颗粒层及多形细胞层厚度,颞叶外颗粒层厚度也处于较低水平,但颞叶外锥体层、内颗粒层及内锥体层厚度最厚。枕叶、额叶、顶叶、颞叶的皮质层的总神经元密度随年龄增长而降低(P0.05),但在30日龄时,枕叶分子层、外颗粒层、外锥体层、内颗粒层和内锥体层的神经元密度、额叶分子层和多形细胞层的神经元密度及颞叶分子层、内颗粒层及内锥体层的神经元密度均处于较高水平。大脑皮质各层厚度及神经元密度的变化规律提示30日龄可能是牦牛的大脑皮质发育变化进而形成低氧适应的关键期。     

山羊胚胎脊髓胶状质的形成和发育

对山羊胚胎脊髓胶状质发育的形态学变化了系统研究，结果表明：（1）山羊脊髓胶状质在胚胎第17周以后逐渐较多的神经元胞体和较大的淡染的神经元细胞核，提示胚胎第17周龄是山羊脊髓胶状质神经元发育的关键时期；（2）山羊脊髓胶状质内神经纤维在胚胎第11周时就已出现，而在髓神经纤维的髓鞘则在胚胎第15周时形成，以后逐渐发育成熟；（3）山羊脊髓胶状质的胶质细胞发育较早，在胚胎第6周末胶状质的胶质细胞发育较早，在胚胎第6周末胶状质原基刚形成时，胶质细胞核已经开始分化，到胚胎第18－19周时，胶质细胞又出现一个增殖高峰。     

Ghrelin在成年皖西白鹅大、小脑内的免疫组化定位

采用免疫组化技术链酶亲和素-生物素-过氧化物酶复合物(StreptAvidin-Biotin-Complex,SABC)法,对成年皖西白鹅大脑和小脑中ghrelin神经元的定位和分布进行了研究。结果显示,大脑分泌ghrelin的神经元和神经纤维主要分布在大脑皮质内,其中锥体层阳性神经元数量最多,多为锥体细胞;小脑分泌ghrelin的神经元主要分布在小脑皮质内,其中蒲肯野细胞层和分子层免疫阳性神经元数量最多,颗粒层阳性神经元数量较少;而大脑和小脑白质内均未见分布。这表明ghrelin在成年皖西白鹅大脑和小脑皮质中分布广泛,可能以自分泌/旁分泌的形式调节中枢神经系统。     

猪大脑皮质、海马结构、梨状叶和杏仁核内leptin长形受体mRNA的分布定位

用分子生物学的方法合成了leptin长形受体（Ob-Rb)反意和正意核酸探针，用原位杂交法研究了5头2-3月龄母猪端脑一些结构内Ob-Rb mRNA的分布定位。结果表明，猪Ob-Rb mRNA分布于大脑皮质、梨状叶、海马、齿状回和杏仁核。大脑皮质和梨状叶内的Ob-Rb mRNA标记神经元主要位于第Ⅱ-Ⅵ层，分子层偶见标记神经元。海马结构内的Ob-Rm mRNA标记神经元主要位于海马的锥体细胞层和齿状回的颗粒层，在海马的始层和齿状回的多形层偶见标记神经元，在海马的辐射层和腔隙层罕见标记细胞。实验结果弥补了猪端脑内Ob-Rb mRNA分布定位资料的空白，为理解leptin的生理功能提供了形态学基础。     

出生前山羊延髓主要灰质核团的形成和发育

对从胚胎期第6周到出生前山羊的延髓主要灰质核团发育的组织学变化进行了系统研究。结果表明：（1）第6周山羊胚胎延髓处在组织发生末期和核团形成初期，是其内部核团构建的关键时期。（2）延髓内不同核团中的神经元发育变化在时间上有较大的差异，在同一核团内神经元胞体发育分化在时间上也有差异，即同一核团内较为成熟的神经元胞体的数量由少到多，细胞质内的尼氏小体也存在由少到多，由小变大的过程。（3）延髓灰质结构形成和神经元发育分化的规律：有些结构发生早，而神经元分化较晚，如下橄榄核、三叉神经脊束核和孤束核；有些结构发生略晚，但其中的神经元胞体分化和发育则较早，如舌下神经核、疑核及延髓的网状结构；有些结构发生早，神经元发育也早，如迷走神经背核。     

nNOS阳性神经元在兔大脑皮质和小脑皮质的分布

利用SABC免疫组织化学方法，对各年龄段家兔大、小脑皮质nNOS阳性神经元的分布和形态结构进行了研究。结果显示：nNOS阳性神经元主要分布在大脑皮质的Ⅱ～Ⅳ层，小脑皮质的颗粒层；nNOS阳性神经元呈深棕色，细胞质明显，细胞核着色较淡，胞体形态多样，有三角形、圆形、椭圆形、梭形等，突起有一个或者数个；阳性神经纤维大多呈棕色串珠样，有些区域的阳性纤维交错分布，相互交织成网状；在大、小脑皮质，阳性神经元密度随年龄增长而逐渐减小，分布变得稀疏，而胞体直径却逐渐增大。由此得出：家兔大脑皮质和小脑皮质内有丰富的nNOS阳性神经元分布，神经元密度随年龄增长逐渐减小，胞体直径逐渐增大；nNOS阳性神经元及其催化产生的NO在家兔中枢神经系统发育和神经调控中起重要作用。     

山羊胎儿脊神经节发育过程中NGF及其受体TrKA的表达

山羊胎儿脊神经节于胚胎第6周就已形成,但此时节内神经元形态不清晰,至第8周,节内神经元形态逐渐清晰,节内神经纤维数量少;随着胚胎发育,节内神经元数量并不显著增加,而是节细胞之间神经纤维及胶质细胞的增多和神经元个体的增长,从而使神经节的体积逐渐增大。节内神经元既可分为形态和着色不同的明暗2类,也可分为细胞直径不同的大、中、小3类。山羊胎儿脊神经节内存在NGF及其受体TrKA,随着胚胎发育,NGF主要分布于节内各类神经元的胞质中,特别是在第14周后;TrKA阳性反应则在第10周后才出现,主要分布于中、小神经元的胞质和胞核,而在大神经元未能见到阳性反应,但在大神经元周围的卫星细胞可观察到TrKA强阳性反应产物。结果提示,NGF对外周神经嵴起源的发育中感觉神经元的生理功能具有重要的调节作用,并与卫星细胞的生长发育和成熟有关。     

nNOS阳性神经元在兔大脑皮质和小脑皮质的分布

利用SABC免疫组织化学方法,对各年龄段家兔大、小脑皮质nNOS阳性神经元的分布和形态结构进行了研究。结果显示:nNOS阳性神经元主要分布在大脑皮质的Ⅱ~Ⅳ层,小脑皮质的颗粒层;nNOS阳性神经元呈深棕色,细胞质明显,细胞核着色较淡,胞体形态多样,有三角形、圆形、椭圆形、梭形等,突起有一个或者数个;阳性神经纤维大多呈棕色串珠样,有些区域的阳性纤维交错分布,相互交织成网状;在大、小脑皮质,阳性神经元密度随年龄增长而逐渐减小,分布变得稀疏,而胞体直径却逐渐增大。由此得出:家兔大脑皮质和小脑皮质内有丰富的nNOS阳性神经元分布,神经元密度随年龄增长逐渐减小,胞体直径逐渐增大;nNOS阳性神经元及其催化产生的NO在家兔中枢神经系统发育和神经调控中起重要作用。     

山羊胚胎大动脉壁发育的组织学研究

本文应用光镜和透射电镜对山羊胚胎大动脉壁的发生发育过程进行了系统观察。结果表明：血管发生初期仅由一层内皮细胞构成。随着胚胎的发育，除毛细血管外，其它血管壁形成分层结构，形成内膜、中膜、外膜；胚胎大动脉内皮细胞胞质内存在着丰富的粗面内质网和游离核糖体，代谢是很活跃的；大动脉管壁的内弹性膜形成较晚，先产生小片段，然后呈连续带状；大动脉内膜和中膜内不含典型的成纤维细胞，在中膜内存在一种能产生胶原纤维的细胞，其结构类似于平滑肌细胞。     

山羊卵泡颗粒细胞和输卵管上皮细胞共培养对山羊体外受精胚胎发育的影响

试验共分 3组 :对照组为单独培养液 ;第 2组为单层颗粒细胞 ;第 3组为输卵管上皮细胞 ,将山羊体外受精胚胎随机放入以上 3组处理中。结果显示山羊体外受精胚胎在卵泡颗粒细胞中发育到囊胚的比率为 4 1.0 % ,在输卵管上皮细胞中发育到囊胚的比率为 5 8.1% ,而在M199培养液中为 5 .6 %。山羊体外受精胚胎分别与山羊卵泡颗粒细胞和输卵管上皮细胞共同培养时 ,均可提高山羊体外受精胚胎的发育进程。且输卵管上皮细胞比颗粒细胞能显著提高山羊体外受精胚胎的发育进程 (P <0 .0 5 )。     

The Neocortex of the Dog

This article describes the structural organization of the neocortex of the dog from purely morphological point of view. Series of 50 urn transverse sections were cut from the frozen right hemiencephala of adult greyhounds, stained by N issl's method, and drawn. His's method was then used to construct life-size lateral, dorsal and medial views of the hemiencephalon from 38 sections located at regular intervals. Once the cytoarchitectonic criteria to be used had been established on the basis of preliminary observations, all the sections of each hemiencephalon were examined microscopically and the cytoarchitectonic types observed in each mapped on the corresponding drawing. These maps were then projected onto lateral, dorsal and medial views of the whole hemiencephalon to produce a classical cytoarchitectonic map of the neocortex made up of 21 types, 7 of them agranular (with no inner granular layer), 2 dysgranular (with a granular layer with diffuse boundans) and the rest granular (with a well-defined layer IV). Various areas of cortex whose characteristics were intermediate between those of adjoinin areas were classified in a residual typus intermedius.     

Polioencephalomalacia in the dog

Disturbance of cerebral blood flow from causes such as meningitis, thromboembolic disease and atherosclerosis was considered an important factor in the pathogenesis of polioencephalomalacia in 25 dogs. In dogs with polioencephalomalacia of undetermined cause, the distribution of lesions in neocortex and paleocortex suggested a change of neuronal metabolism secondary to cerebral anoxia/ischemia. Five dogs with canine distemper infection had bilateral necrosis of the hippocampus and pyriform cortex. Convulsions, central visual impairment and hemiparesis were the most prominent neurologic signs.     

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.     

Prenatal development of the adrenal gland in the one-humped camel (Camelus dromedarius)

With 14 figures and 3 tables SUMMARY: Each adrenal gland consisted of cortex and medulla that developed from different embryological origins and presented different cellular organization. One hundred male or female camel embryos or fetuses with crown vertebral rump lengths (CVRL) that ranged from 0.8 to 117 cm were examined. The adrenal cortex, which is derived from intermediate mesoderm, was first observed in the 0.8-cm CVRL camel embryo. The adrenal cortex initially was combined with the gonad as a thickened region of proliferating cells derived from splanchnic intermediate mesoderm. Adrenocortical tissue was first separated from the gonadal tissue in the 2-cm CVRL camel fetus and was observed as a separate dorso-medial mass of cells. At 2.5-cm CVRL, the adrenocortical tissue was surrounded by a capsule of undifferentiated mesenchymal cells, except at its proximal pole, where an invagination was located through which chromaffinoblast cells entered the cortex. The chromaffinoblast cells migrated from the neural crest to form the medulla of the developing adrenal gland. In the 3.5-cm CVRL camel fetus, the adrenocortical cells differentiated into two layers: the inner fetal cortex and the outer definitive cortex. As development proceeded, the fetal cortex degenerated and the definitive cortex formed the zona glomerulosa and zona fasciculata. The zona reticularis did not form until the end of gestation. During prenatal life, the adrenal medulla was much thicker than the cortex.     

Effect of methotrexate on cerebellar development in infant rats

Six-day-old rats were treated intraperitoneal injections with methotrexate 1 mg/kg, and the cerebellum was examined. Both the length and width of the vermis decreased in the methotrexate-treated group instead of the control from 4 day after treatment (DAT) onward. A significant reduction in the width of the external granular layer was detected on 2 and 3 DAT in the methotrexate group. By 4 DAT, the width of the external granular layer of the methotrexate group was indistinguishable from the control, and by 8 DAT, it was greater than that of the control. The molecular layer of methotrexate group on 8 and 15 DAT was thinner than that of the control. On 1 DAT, in the methotrexate group, there were many TUNEL and cleaved caspase-3-positive granular cells throughout the external granular layer, and they decreased time-dependently. On 1 DAT, in the methotrexate group, phospho-histone H3-positive cells in the external granular layer were fewer than in the control and tended to increase on 2–4 DAT. The p21-positive-rate of the external granule cells in the MTX group was higher than in the control on 1–4 DAT. These results suggested that methotrexate exposure on postnatal day 6 induces a delay, slowing in the migration of external granular cells to the inner granular layer, attributed to decrease or inhibition in the production of external granular cells that had arisen from apoptosis and the decrease in cell proliferative activity, resulting in cerebellar hypoplasia.     

Development of the Retina in the Porcine Fetus A Light Microscopic Study

Morphogenesis of the porcine retina was studied using light microscopy from 4 weeks of gestation until birth (18 to 310 mm crown-rump length), and compared with the adult stage (6 months). Tissue samples were examined from the posterior and peripheral parts of the retina. At 18 mm the retina consists of an inner marginal layer and an outer layer of neuroblastic cells. At 18-40 mm the latter layer is divided into an inner and an outer neuroblastic layer by the transient layer of Chievitz. Subsequently, the development of the different retinal layers begins at the inner retinal border and moves progressively outwards; it also spreads from the posterior to the peripheral part of the neural retina. Many cells of the inner neuroblastic layer are prospective ganglionic cells which migrate inwards, thus forming the ganglion cell layer and the inner plexiform layer at 90 mm. At 120 mm, primitive horizontal cells appear within the outer neuroblastic layer. Separation of this layer into the inner nuclear, outer plexiform and outer nuclear layers is first evident at 180 mm. At this stage all retinal layers are present, except the layer of the photoreceptor cells which is not widespread until at 220 mm. The inner and outer segments of the photoreceptor cells lengthen considerably during the last month of gestation. During the late fetal stage the nerve fiber layer, the inner and outer plexiform layers and the layer of rods and cones all continue to increase in thickness. Concurrently, the ganglion cell layer and the inner and outer nuclear layers have reached their maximal thickness and become thinner. After the total thickness of the neural retina amounts to approximately 180 microns at two to three weeks before birth, it then thins to approximately 160 microns in the adult stage.     

Granulomatous encephalitis in a neurologically impaired goat kid associated with degeneration of Neospora caninum tissue cysts.

Congenital Neospora caninum infection was diagnosed in a Saanen goat from a farm in southern Brazil. The kid was unable to nurse and had difficulty rising, ataxia, and opistothotonos. The neurologic signs became more severe 3 days after birth, when it was euthanized. No gross lesions were observed at necropsy. Multifocal infiltrates primarily of mononuclear cells, nodular microgliosis, and perivascular cuffs of lymphocytes, plasma cells, and few neutrophils were observed in the brain, mostly in the cortex and adjacent to ventricles. Rare multinucleate giant cells were observed adjacent to inflammatory foci. Several tissue cysts with a thick wall that reacted strongly with polyclonal antiserum to N. caninum were in the cerebral cortex and medulla oblongata. Lesions were also present in heart, lungs, and liver, but N. caninum tachyzoites were not found. Distinguishing features in this goat kid included neurologic impairment resulting from congenital infection with N. caninum and the presence of granulomatous inflammation with rare giant cells associated with degeneration of tissue cysts.     

Caprine beta-mannosidosis: phenotypic features

The clinical features of caprine beta-mannosidosis were evaluated in 10 newborn goats, one stillborn goat and one goat fetus. The phenotypic abnormalities observed in all 10 live affected animals included an inability to rise from a recumbent position, moderate to marked intention tremor, eye movements resembling pendular nystagmus, clinical deafness, bilateral Horner's syndrome, carpal contractures, pastern joint hyperextension, thickened skin and to a varying degree, a dome-shaped skull. Subjective evaluation suggested that most animals had a decreased muscle mass. Together, these characteristics represent a common phenotype which is expressed at birth in caprine beta-mannosidosis.     

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.     

Two cases of hereditary quadriplegia and amblyopia in a litter of Irish setters

Two, one-month-old male Irish setters from the same litter showed incoordination, rotary nystagmus and motor and visual impairment. No abnormalities were found in either the blood, urine or cerebrospinal fluid. Radiographs of the head, chest and abdomen were normal. Histopathology revealed degeneration and necrosis of the granular layer and Purkinje cells of the cerebellar cortex. On electron microscopic examination, the granular cells showed dilated endoplasmic reticulum and vacuolated mitochondrial cristae. There was also serious destruction of Purkinje cells.