猫腰髓白质年龄相关的形态学变化

以青年成年猫(1-3龄,2-2．5 kg)和老年猫(12龄,3-3．5kg)L6段脊髓白质为研究对象,用 神经丝蛋白(NF)免疫染色显示神经纤维,用改良的Holzer结晶紫染色显示所有胶质细胞并用成年动物Golgi 法显示其形态,用胶质纤维酸性蛋白(GFAP)免疫染色显示星形胶质细胞。光镜下对青年猫与老年猫腰髓白质 中神经纤维和胶质细胞进行形态学观察和定量研究。与青年猫相比,老年猫腰髓白质中的神经纤维密度显著下 降(P相似文献   

猫小脑髓质胶质反应的年龄相关性变化

探讨青年猫和老年猫小脑髓质中胶质反应的年龄相关性变化及其意义。用改良的Holzer结晶紫染色显示所有胶质细胞,GFAP(胶质纤维酸性蛋白)免疫染色显示星形胶质细胞。光镜下对青年猫与老年猫小脑髓质中胶质细胞和GFAP免疫阳性(GFAP-IR)星形胶质细胞进行形态学观察和定量研究。与青年猫比较,老年猫小脑髓质中胶质细胞和GFAP-IR细胞密度均显著增加(P<0.01),胞体较大;GFAP阳性细胞阳性反应较强,突起稠密;星形胶质细胞占胶质细胞总数比例增加。这表明小脑髓质中胶质细胞随年龄增长明显增生,尤其星形胶质细胞具有明显的年龄相关性活动增强。提示胶质细胞及星形胶质细胞的增生可能对衰老的神经纤维起保护作用;星形胶质细胞对衰老较敏感。     

青年猫和老年猫视神经超微结构观察比较

目的探讨青年猫和老年猫视神经年龄相关的形态学变化及可能造成的生理影响。方法取4只青年猫(2-3岁,2-2.5kg)和4只老年猫(10-13岁,2.5-3.5kg)颅内相对应部分视神经,制作横向半薄切片和超薄切片,半薄切片用甲苯胺蓝硼砂溶液染色,光镜观察、测量视神经的直径(不含外层神经膜);超薄切片标本用醋酸和柠檬酸铅染色,电镜观察、计数视神经纤维密度、测量视神经纤维外径D(含髓鞘)和内径d(不含髓鞘),按一定分级范围算出各种直径的纤维及各种d/D比值的纤维所占百分比,分别画出直方图,对实验结果进行统计学分析并绘制纤维直径谱。结果与青年猫相比,老年猫视神经直径显著增大(P0.05);纤维数量显著下降(P0.05)。纤维直径谱分析结果显示,青、老年猫纤维直径分布范围相似,但老年猫纤维的峰直径及纤维平均直径比青年猫的显著减小(P0.05),老年猫视神经纤维的d/D比值亦明显降低。另外,老年猫视神经中部分轴突肿胀,髓鞘疏松、结构紊乱,板层脱离、空泡化,有的轴索髓鞘溶解。结论在衰老过程中,老年猫视神经纤维丢失,纤维直径减小,d/D比值下降,以及纤维髓鞘的松散解体,这些变化均可能导致视神经纤维对视觉信息的传导速度减慢,是老年个体视觉分析速度下降的重要原因。     

猫视神经中S100蛋白表达的年龄相关变化

比较老年猫和青年猫视神经S100蛋白表达及胶质细胞的年龄相关变化,探讨其可能的生理作用.取老年猫(10～13龄)和青年猫(1～3龄)各4只的颅内视神经相应部分作组织切片,用免疫组织化学ABC法标记S100免疫阳性(S100～IR)细胞,Marsland-Gless染色显示胶质细胞.光镜下采用图像分析系统计数视神经中S100-IR细胞密度、胶质细胞密度及阳性反应灰度值.视神经中棕黄色S100-IR细胞分布均匀,Marsland-Gless染色的纤维横断面及胶质细胞均呈棕红色.与青年猫相比,老年猫视神经中胶质细胞密度明显增大;S100-IR细胞密度显著增加(P<0.01),胞体较大,阳性较强(灰度值显著减小,P<0.01);S100-IR细胞在胶质细胞中所占比例亦显著增大.结果表明S100-IR细胞呈明显的年龄相关性增生,这可能对衰老的神经纤维起保护作用.     

猫视皮层星形胶质细胞的老年性变化

电生理研究结果显示,在衰老过程中猫的视皮层神经元对视觉刺激的反应性出现显著的功能衰退,是否这种功能性衰退伴随胶质细胞活动的改变尚无直接的实验证据。以前期电生理实验猫为材料,用免疫形态学方法比较青年猫和老年猫初级视皮层内星形胶质细胞的活动状况。利用Nissl染色显示猫初级视皮层组织结构,用免疫组织化学方法（SABC法）显示GFAP免疫阳性（GFAP-IR）星形胶质细胞。光镜下观察、拍照,对GFAP-IR细胞计数并换算成密度,测量GFAP-IR直径取平均值。老年猫初级视皮层灰质各层及白质内的GFAP-IR细胞密度比青年猫的显著升高（p〈0.001）。与青年猫相比,老年猫视皮层灰质和白质中GFAP-IR细胞的平均直径均比青年猫的显著增大（p〈0.0001）,且老年猫视皮层内GFAP阳性免疫反应较青年猫的明显增强。老年猫初级视皮层神经元功能衰退伴随着星形胶质细胞活动的增强,胶质细胞活动增强有助于神经元之间的信息交流,因而可能对衰老过程中神经元的功能衰退起补偿作用。     

猫视网膜年龄相关的形态学变化

取老年猫(12龄,3～3．5kg)和青年猫(1～3龄,2～2．5kg)各4只的视网膜,经4％多聚甲醛处理后,用H．E．染色以显示视网膜结构,Nissl染色显示神经节细胞,免疫组织化学ABC法染色以显示星形胶质细胞特征性标志物胶质纤维酸性蛋白(GFAP)的阳性反应细胞的分布。显微镜下观察测量视网膜厚度,计数神经节细胞、GFAP免疫反应阳性细胞数。与青年猫比较,老年猫视网膜总厚度以及外核层、外网状层、内核层和内网状层厚度均显著减小;神经节细胞层的细胞密度显著下降;GFAP免疫反应阳性细胞显著增加,GFAP阳性细胞阳性反应强,胞体明显膨胀,突起稠密粗大。推测在衰老过程中视网膜细胞有神经元丢失现象,可能是造成视觉功能衰退的重要原因之一;视网膜星形胶质细胞的功能增强可能会延缓衰老。     

猫下丘中央核5-HT、P物质和星形胶质细胞年龄相关变化

目的比较研究青年猫与老年猫下丘中央核(CIC)5-羟色氨(5-HT)、P物质(SP)能神经元及星形胶质细胞年龄性变化,探索老年个体听力下降的神经机制。方法 Nissl染色显示下丘神经元,免疫组织化学ABC法显示5-HT、SP和胶质纤维酸性蛋白(GFAP)免疫反应(immunoreactive,IR)细胞。光镜下观察、拍照,对神经元和5-HT、SP及GFAP免疫反应细胞分别计数并换算成密度,测量其IR细胞直径取平均值,以及它们的阳性反应平均灰度值。结果 5-HT-IR、SP-IR和GFAP-IR细胞、阳性纤维及其终末在青年猫及老年猫下丘中央核均有分布。与青年猫相比,老年猫下丘中央核5-HT密度均显著下降(P<0.01),胞体直径明显减小(P<0.01),阳性反应明显减弱(阳性反应强度与灰度值呈负相关),SP-IR神经元和星形胶质细胞密度却显著增大,阳性反应显著增强。结论在衰老过程中猫下丘神经元尤其是5-HT能神经元有显著丢失现象,提示5-HT能神经元显著减少导致下丘听觉信息传递功能减弱,可能引起老年个体听觉功能衰退的重要原因;SP能神经元和星形胶质细胞密度显著增大,可能起到延缓衰老的作用。     

视神经年龄相关的形态学变化研究进展

处于衰老过程中的视神经呈现出年龄相关变化。主要包括视神经纤维髓鞘的老化崩解、纤维显著丢失、纤维直径减小及其对兴奋的传导速度减慢;视神经胶质细胞显著增生。视神经纤维衰老性改变可能导致视觉功能的衰退;胶质细胞的增生可能对维持视神经的形态及延缓视神经进一步衰老起保护作用。     

猫运动皮层神经元和S100、GFAP阳性细胞的年龄相关性变化

比较了青、老年猫运动皮层神经元与S100、GFAP免疫阳性胶质细胞的形态学变化,并探讨其与衰老过程中运动功能衰退的关系。采用Nissl染色显示青、老年猫运动皮层分层结构和神经元。免疫组织化学方法（SABC法）显示青、老年猫运动皮层S100免疫反应阳性(S100-immunoreactive, S100-IR)细胞及胶质纤维酸性蛋白免疫反应阳性(GFAP-immunoreactive, GFAP-IR)细胞。在Olympus 显微镜下,用Moitcam 5000数码成像与分析系统计数运动皮层各层神经元、S100-IR细胞及GFAP-IR细胞的数量,并随机抽样测量S100-IR、GFAP-IR细胞的胞体直径。与青年猫相比,老年猫运动皮层Ⅴ、Ⅵ层神经元密度显著下降(P < 0.01),老年猫运动皮层中S100-IR和GFAP-IR细胞密度与胞体直径均显著增加(P < 0.01),且细胞的免疫阳性反应较强。研究结果表明,猫运动皮层的神经元密度在衰老过程中Ⅴ、Ⅵ层神经元密度显著下降,有可能会降低老年个体运动皮层对运动的调控能力;随着衰老、运动皮层的星形胶质细胞出现明显的反应性活化与增生,这对维持大脑运动皮层神经元的活性和神经元之间的通讯联系,从而延缓老年性运动功能衰退具有重要意义。     

猫运动皮层神经元和S100、GFAP阳性细胞的年龄相关性变化

比较了青、老年猫运动皮层神经元与S100、GFAP免疫阳性胶质细胞的形态学变化,并探讨其与衰老过程中运动功能衰退的关系。采用Nissl染色显示青、老年猫运动皮层分层结构和神经元。免疫组织化学方法(SABC法)显示青、老年猫运动皮层S100免疫反应阳性(S100-immunoreactive,S100-IR)细胞及胶质纤维酸性蛋白免疫反应阳性(GFAP-immunoreactive,GFAP-IR)细胞。在Olympus显微镜下,用Moitcam5000数码成像与分析系统计数运动皮层各层神经元、S100-IR细胞及GFAP-IR细胞的数量,并随机抽样测量S100-IR、GFAP-IR细胞的胞体直径。与青年猫相比,老年猫运动皮层Ⅴ、Ⅵ层神经元密度显著下降(P<0.01),老年猫运动皮层中S100-IR和GFAP-IR细胞密度与胞体直径均显著增加(P<0.01),且细胞的免疫阳性反应较强。研究结果表明,猫运动皮层的神经元密度在衰老过程中Ⅴ、Ⅵ层神经元密度显著下降,有可能会降低老年个体运动皮层对运动的调控能力;随着衰老、运动皮层的星形胶质细胞出现明显的反应性活化与增生,这对维持大脑运动皮层神经元的活性和神经元之间的通讯联系,从而延缓老年性运动功能衰退具有重要意义。     

猫下丘中央核GABA能神经元年龄相关变化

目的比较研究猫下丘中央核(CIC)GABA能神经元年龄相关变化,探索老年个体听力下降的神经机制。方法Nissl染色显示下丘神经元,免疫组织化学ABC法显示γ-氨基丁酸(GABA)免疫阳性神经元。光镜下观察、拍照,对神经元和GABA能神经元分别计数并换算成密度,测量GABA能神经元直径取平均值。结果GABA阳性反应神经元、阳性纤维及其终末在青年猫及老年猫下丘中央核均有分布。与青年猫相比,老年猫下丘中央核神经元及GABA能神经元密度均显著下降(P<0.01),GABA能神经元下降幅度较大;GABA能神经元胞体直径明显减小(P<0.01),阳性反应明显减弱。结论在衰老过程中猫下丘神经元尤其是GABA能神经元有显著丢失现象,提示GABA能神经元显著减少导致下丘兴奋性和抑制性神经递质之间的平衡失调,可能是引起老年个体听觉功能衰退的重要原因。     

猫嗅球外丛层和僧帽细胞层年龄相关形态学变化

分别用Nissl法及免疫组织化学ABC法标记青、老年猫嗅球中嗅觉二级神经元和外丛层胶质细胞,显微镜下观察其分布并计数,对嗅觉二级神经元胞体直径和外丛层厚度进行测量,比较其年龄相关性变化,研究神经元与胶质细胞之间的关系,探讨老年性嗅觉功能衰退的相关神经机理。结果显示,老年猫嗅觉二级神经元胞体直径和分布密度均有不同程度的显著性下降(P<0.05);外丛层厚度变化不明显(P>0.05);外丛层胶质细胞特别是星形胶质细胞显著性增生(P<0.05)。表明在衰老过程中嗅觉二级神经元有丢失,并呈现功能下降,可能是老年性嗅觉功能衰退的原因之一。同时外丛层胶质细胞增生以进一步保护神经元,延缓其衰老。     

Molecular structure of the axolemma of developing axons following altered gliogenesis in rat optic nerve

Axonal and axolemmal development of fibers from rat optic nerves in which gliogenesis was severely delayed by systemic injection of 5-azacytidine (5-AZ) was examined by freeze-fracture electron microscopy. In neonatal (0-2 days) rat optic nerves, all fibers lack myelin, whereas in the adult, virtually all axons are myelinated. The axolemma of neonatal premyelinated fibers is relatively undifferentiated. The P-fracture face (P-face) displays a moderate (approximately 550/micron 2) density of intramembranous particles (IMPs), whereas the E-fracture face (E-face) has few IMPs (approximately 125/micron 2) present. By 14 days of age, approximately 25% of the axons within control optic nerves are ensheathed or myelinated, with the remaining axons premyelinated. The ensheathed and myelinated fibers display increased axonal diameter compared to premyelinated axons, and these larger caliber fibers exhibit marked axonal membrane differentiation. Notably, the P-face IMP density of ensheathed and myelinated fibers is substantially increased compared to premyelinated axolemma, and, at nodes of Ranvier, the density of E-face particles is moderately high (approximately 1300/micron 2), in comparison to internodal or premyelinated E-face axolemma. In optic nerves from 14-day-old 5-AZ-treated rats, few oligodendrocytes are present, and the percentage of myelinated fibers is markedly reduced. Despite delayed gliogenesis, some unensheathed axons within 5-AZ-treated optic nerves display an increased axonal diameter compared to premyelinated fibers. Most of these large caliber fibers also exhibit a substantial increase in P-face IMP density. Small (less than 0.4 micron) diameter unensheathed axons within treated optic nerves maintain a P-face IMP density similar to that of control premyelinated fibers. Regions of increased E-face particle density were not observed. The results demonstrate that some aspects of axolemma differentiation continue despite delayed gliogenesis and the absence of glial ensheathment, and suggest that axolemmal ultrastructure is, at least in part, independent of glial cell association.     

The ultrastructure of the cardiac ganglion of the desert scorpion,Paruroctonus mesaensis (Scorpionida: Vaejovidae)

Light and electron microscopy of the pacemaker ganglion of the scorpion heart indicate that it is about 15 mm long and 50 μm in diameter and extends along the dorsal midline of the heart. The largest cell bodies (30–45 μm in diameter) occur in clusters along the length of the ganglion. The ganglion appears to be innervated with fibers from the subesophageal and first three abdominal ganglia. The cardiac ganglion is surrounded by a neurilemma and a membranous sheath. The latter is apparently derived from connective tissue cells seen outside the ganglion. Nerve fibers other than those in the neuropil areas are usually surrounded by membrane and cytoplasm of glial cells. Often there are several layers of glial membrane, forming a loose myelin. The cardiac nerves to the heart muscle are also surrounded by a neurilemma, and the axons are surrounded by glia. The motor nerves contain lucent vesicles 60–100 nm and opaque granules 120–180 nm in diameter. In the cardiac ganglion, some nerve cell bodies have complex invaginations of glial processes forming a peripheral trophospongium. In the neuropil areas, nerve cell processes are often in close apposition. The septilaminar configuration typical of gap junctions is common, with gap distances of 1–4 nm. In tissues stained with lanthanum phosphate during fixation, we found gaps with unstained connections (1–2 nm diameter) between nerve-nerve and glial-nerve cell processes. Annular or double-membrane vesicles in various stages of formation were also seen in some nerve fibers in ganglia stained with lanthanum phosphate. Nerve endings with electron-lucent vesicles 40–60 nm in diameter are abundant in the cardiac ganglion, suggesting that these contain the excitatory transmitter of intrinsic neurons of the ganglion. Less abundant are fibers with membrane-limited opaque granules, circular or oblong in shape and as much as 330 nm in their longest dimension. Also seen were some nerve endings with both vesicles and granules.     

Molecular and cellular aspects of axon-glia interaction in CNS regeneration

The relationships of neurons and non-neuronal cells are vital for the maintenance and function of neurons. Trauma alters these relationships causing proliferation of non-neuronal cells and, in adult mammalian CNS, presumably disturbs the environmental support needed for regeneration. A supportive environment can be restored by introducing a regenerating nerve to injured mammalian CNS. This response is probably due, at least in part, to diffusible substances secreted by the non-neuronal cells. We have obtained diffusible substances from either regenerating fish optic nerves or neonatal rabbit optic nerves and applied them around crushed adult rabbit optic nerves. This manipulation caused the adult nerve to show regenerative changes: a general increase of protein synthesis in the retinas; selective increase in synthesis of a few polypeptides in the retinas; sprouting from the retinas in vitro; increased viability of nerve fibers as shown by HRP staining; and the appearance of growth cones adjacent to glial limitans in the injured nerves. We termed these diffusible, active substances "Growth Associated Triggering Factors" (GATFs). In addition to the phenomena described above, the active substances (obtained in the form of media conditioned by regenerating fish optic nerve or neonatal rabbit optic nerve) caused various other changes in the injured nerve itself: acceleration of non-neuronal cell proliferation; changes in the protein pattern, e.g. an increase in a 12 kDa polypeptide which might be a second mediator in the cascade of events leading to regeneration; increased laminin immunoreactive sites in the nerve; and the acquisition of growth supportive activity in media conditioned by the implanted injured nerves.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dolphin peripheral visual pathway in chronic unilateral ocular atrophy: Complete decussation apparent

Components of the peripheral visual pathway were examined in two bottlenose dolphins, Tursiops truncatus, each with unilateral ocular degeneration and scarring of 3 or more years' duration. In both animals, the optic nerve associated with the blind eye right eye in Tg419 and left eye in Tt038 had a translucent, gel-like appearance upon gross examination. This translucency was also evident in the optic tract contralateral to the affected eye. In Tg419, myelinated axons of varying diameters were apparent in the left optic nerve, whereas the right optic nerve, serving the blind eye, appeared to be devoid of axons. In Tt038, myelinated axons were associated with the right optic nerve (serving the functional eye) and left optic tract but were essentially absent in the left optic nerve and right optic tract. Examined by light microscopy in serial horizontal sections, the optic chiasm of Tt038 was arranged along its central plane in segregated, alternating pathways for the decussation of right and left optic nerve fibers. Ventral to this plane, the chiasm was comprised of fibers from the left optic nerve, whereas dorsal to the central plane, fibers derived from the right optic nerve. Because of this architectural arrangement, the right and left optic nerves grossly appeared to overlap as they crossed the optic chiasm with the right optic nerve coursing dorsally to the left optic nerve. At the light and electron microscopic levels, the optic nerves and tracts lacking axons were well vascularized and dominated by glial cell bodies and glial processes, an expression of the marked glial scarring associated with postinjury axonal degeneration. The apparent absence of axons in one of the optic tract pairs (right in Tt038 and left in Tg419) supports the concept of complete decussation of right and left optic nerve fibers at the optic chiasm in the bottlenose dolphin. © 1994 Wiley-Liss, Inc.     

The Fine Anatomy of the Optic Nerve of Anurans—An Electron Microscope Study

In the optic nerve of Anurans numerous myelinated and unmyelinated axons appear under the electron microscope as compact bundles that are closely bounded by one or several glial cells. In these bundles the unmyelinated fibers (0.15 to 0.6 µ in diameter) are many times more numerous than the myelinated fibers, and are separated from each other, from the bounding glial cells, or from adjacent myelin sheaths, by an extracellular gap that is 90 to 250 A wide. This intercellular space is continuous with the extracellular space in the periphery of the nerve through the numerous mesaxons and cell boundaries which reach the surface. Numerous desmosomes reinforce the attachments of adjacent glial membranes. The myelinated axons do not follow any preferential course and, like the unmyelinated ones, have a sinuous path, continuously shifting their relative position and passing from one bundle to another. At the nodes of Ranvier they behave entirely like unmyelinated axons in their relations to the surrounding cells. At the internodes they lie between the unmyelinated axons without showing an obvious myelogenic connection with the surrounding glial cells. In the absence of connective tissue separating individual myelinated fibers and with each glial cell simultaneously related to many axons, this myelogenic connection is highly distorted by other passing fibers and is very difficult to demonstrate. However, the mode of ending of the myelin layers at the nodes of Ranvier and the spiral disposition of the myelin layers indicate that myelination of these fibers occurs by a process similar to that of peripheral nerves. There are no incisures of Schmidt-Lantermann in the optic myelinated fibers.