与眶下神经相关的初级传入纤维终末的溃变、非突触部位胞吐及突触联系

切断眶下神经的各组大鼠存活2～30天后分别杀死,于其三叉神经尾侧脊束核胶状质亚核内观察了一级传入纤维轴突终末的溃变过程.非突触部位胞吐及突触联系.结果发现:(1)眶下神经的跨节溃变、以突触小泡聚集、融合、空泡形成为主要特征,无微丝增生现象:(2)部分溃变终末内的线粒体明显肿胀变暗.呈球形改变:(3)大致密核心小泡的溃变时间远滞后于突触小泡.两者并不同步进行;(4)轴突终未在溃变过程中,其内的大致密核心小泡仍然进行非突触部位胞吐;(5)溃变纤维终末于胶状质内分别形成轴一树、轴一体、轴一轴三种类型的突触、并参与了突触复合体的形成.     

Ultrastructural changes of the central scalloped (C1) primary afferent endings of synaptic glomeruli in the substantia gelatinosa Rolandi of the rat after peripheral neurotomy

Summary Fine structural changes were observed in the dark scalloped central C₁ terminals of type I synaptic glomeruli in spinal cord segments C6–C7 of the rat 3 days after cutting the three main forelimb nerves. Twenty-six per cent of the C₁ terminals occurring on the ipsilateral side showed a lighter appearance due to a decrease in the number of synaptic vesicles. The number of synaptic vesicles per unit section area was only 42% of that present in normal C₁ terminals on the contralateral side. The number of synaptic contacts of C₁ terminals with the profiles surrounding them in each glomerulus was diminished and glial envelopment was increased to 15% of C₁ terminal contour. Up to day 12, vesicle and synaptic losses were gradually aggravated and glial apposition was increased, but no obvious signs of glial engulfment were observed. From day 3 to day 12, altered C₁ terminals increased in number, while those that appeared normal decreased. The latter had disappeared at day 12 and the altered ones at day 15, and from this stage type I glomeruli were no longer present on the treated side. The lack of electron-dense degenerative bouton changes characteristic of Wallerian degeneration offers an explanation for the lack of or minimal amount of argyrophilic structures which has been found consistently in the substantia gelatinosa during transganglionic degeneration. The gradual decay of the C₁ terminals raises the question of their fate. Future studies with the use of a stable marker might provide an answer.     

An ultrastructural study of nerve terminal degeneration in muscle spindles of the tenuissimus muscle of the cat

Summary Muscle spindles in the tenuissimus muscle of the cat were studied between 12 and 168 h after cutting or freezing the nerve to this muscle. Degenerative changes in sensory and motor nerve terminals on intrafusal muscle fibres were observed using the electron microscope. Comparisons were made with spindles from unoperated or sham-operated cats.The earliest degenerative changes were seen in sensory and motor terminals at 20–24 h after the lesion. No nerve endings were seen by 114 h after denervation. The most consistent initial signs of degeneration were: (1) the presence of abnormal mitochondria and dense bodies in sensory terminals, and (2) a decrease in the number and clumping of synaptic vesicles combined with an increase in glycogen and neurofilaments in motor endings. Intrafusal fibres participate in the removal of degenerating sensory endings. Schwann cells phagocytose degenerating motor terminals. The disappearance of nerve terminals precedes the complete degeneration of preterminal myelinated fibres within the muscle spindle.     

The action of capsaicin on primary afferent central terminals in the superficial dorsal horn of newborn mice

Capsaicin was injected subcutaneously (50 mg/kg) into 10 mice on days 2 or 3 after birth, and 12 h, 3 and 5 days later the distribution and structure of degenerated primary afferent central axons or terminals (C-terminals) in the lumbar spinal dorsal horn were examined by electron microscopy. Degenerated terminal axons with dense or lamellar bodies or higher electron density were conspicuous 12 h after treatment with capsaicin. Severely degenerated unmyelinated axons, including dense or lamellar bodies engulfed by microglial cells, were numerous in the most superficial (marginal) layer, but rarely seen in the substantia gelatinosa. Two types of primary afferent central terminals in the substantia gelatinosa showed various extents of degeneration: small dark C-terminals (CI-terminals) with densely packed agranular synaptic vesicles, and large light ones (CII-terminals) with less dense agranular synaptic vesicles and a few granular synaptic vesicles. Thus, many central axon terminals of dorsal root ganglion (DRG) neurons that are sensitive to capsaicin enter the marginal layer and substantia gelatinosa. Degenerated primary afferent central axons or terminals markedly decreased in the superficial dorsal horn 3 and 5 days after capsaicin treatment, still, there were many degenerating DRG neurons at this time as shown by our previous study. Previously we also reported that fewer slightly degenerating unmyelinated dorsal root axons and small DRG neurons appear at 12 h and larger DRG neurons degenerate later than smaller ones after treatment with capsaicin. As a result, the discovery of many severely degenerated terminal axons in the superficial dorsal horn soon after treatment supports the idea that capsaicin first acts on the central terminals and that this is followed by damage to larger DRG neurons.     

Projections of ventromedial hypothalamic neurons to the midbrain central gray: an ultrastructural study

Ventromedial hypothalamic projections to the midbrain central gray may be involved in the mediation of female reproductive behavior. In order to demonstrate and examine projections of the ventromedial nucleus in the midbrain central gray, in the rat, electrolytic lesions were placed in the ventromedial nucleus and the midbrain central gray was examined for ultrastructural signs of degeneration at various intervals, i.e. 27.5 h and two, four, six and eight days following the lesions. The fine structure of the midbrain central gray of unlesioned animals was also examined to characterize its normal morphology and to establish a baseline with which to compare the effects of the lesion. In unlesioned animals, the neuropil of midbrain central gray contained several synaptic types, with axodendritic synapses appearing to be the most predominant. Dendrites contained well-preserved microtubules. Synaptic endings contained many clear, round vesicles and some contained dense-cored vesicles as well. Neuropil synapses were both asymmetric and symmetric. Cell bodies were characterized by light cytoplasm and had asymmetric and symmetric synapses on their surface. Following electrolytic lesions in the ventromedial nucleus, various types of degenerative patterns were seen in the midbrain central gray, including electron-dense, flocculent, watery, and pinocytotic degeneration. Specific characteristics of degeneration included shrunken, dense axons and endings, clumped synaptic vesicles, abnormally large, dark mitochondria, membranous sacs of various sizes, swollen endings with reduced numbers of synaptic vesicles, and endings and processes containing large numbers of coated vesicles. Some of these signs were already evident at 27.5 h following the lesion. In addition, degenerating postsynaptic processes and cell bodies were seen in the midbrain central gray. At 27.5 h survival time, degenerating dendritic processes often appeared swollen, devoid of microtubules, and contained enlarged mitochondria. At longer survival times neuronal degeneration was observed in the midbrain central gray, characterized by electron-dense cell bodies and pycnotic nuclei. Both degenerating pre- and postsynaptic elements appeared to be engulfed by glial processes. Control lesions in non-hypothalamic regions which project to the midbrain central gray, i.e. nucleus gigantocellularis and pontine reticular formation and in a non-projecting region, i.e. parietal cortex, were performed.(ABSTRACT TRUNCATED AT 400 WORDS)     

皮质—小脑前核—小脑通路—HRP法结合溃变电镜法研究

目的：观察大鼠小脑前核（桥核,下橄榄,外侧网状核,桥被盖网状核和旁正中网状核）中皮质纤维终末的溃变型及其与各核中的小脑投射神经元的突触联系。材料和方法：８只大鼠,用ＨＲＰ逆行示记法和溃变电镜技术。结果：（１）溃变型有三种,电子致密型,微丝增生型以及电子透明型。（２）电子致密型溃变有三种不同形态,即含圆形清亮型小泡,含多形清亮型小泡和混合型小泡的三种终末,其中绝大多数溃变终末含圆形亮型小泡。（４）溃     

Comparative ultrastructural neuropathology of naturally occurring bovine spongiform encephalopathy and experimentally induced scrapie and Creutzfeldt-Jakob disease.

We report the ultrastructural neuropathology of bovine spongiform encephalopathy (BSE), a recently described slow virus disease first recognized in Friesian/Holstein cattle, and compare it to that of experimental scrapie and Creutzfeldt-Jakob disease. The spongiform change, which was most pronounced in the central grey matter of the midbrain, consisted of membrane-bound vacuoles within neuronal processes, containing curled membrane fragments, secondary chambers and vesicles. Axons and dendrites accumulated whorls of neurofilaments and other subcellular organelles, such as mitochondria and dense bodies, which were entrapped within the filamentous masses. Other neurites accumulated electron-dense bodies, and still others electron-lucent cisterns and branching tubules. Membrane-bound neuronal inclusions, composed of tubules measuring 10 nm in diameter, were found in axonal terminals. Tubulovesicular structures were loosely packed and were occasionally surrounded by a common membrane, a finding previously described only in natural scrapie in sheep. Except for the intraneuronal inclusions, all of the ultrastructural features of BSE resembled those found in scrapie and Creutzfeldt-Jakob disease.     

Observations on the process of degeneration of the afferent connections to the sensori-motor cortex of the monkey.

The ultrastructural features of degeneration of the afferent connections to the sensorimotor cortex of the primate have been studied with the electron microscope. Thalamo-cortical terminals show cytoplasmic darkening and swelling of vesicles, and neurofilaments and glycogen are often prominent in the larger terminals, although true neurofilamentous hypertrophy is rare. The terminals of the commissural and association projections similarly show darkening and some swelling of vesicles but are usually smaller and neurofilaments and glycogen are rarely seen. Ethanolic-phosphotungstic acid specifically stains degenerating axons and axon terminals. Degeneration occurs more rapidly in the terminals of the association projections than in those of the longer commissural projection although terminals at different stages of degeneration are present simultaneously in both instances. Micropinocytosis of degenerating terminals has been found and both glial and neuronal profiles are involved in this. Exposed post-synaptic thickenings have been seen and these induce subsurface cisternae in the neuronal structures to which they become apposed, including axon initial segments and unmyelinated axons.Damage to a part of the central nervous system thus causes consequential changes in other regions, and these changes are relevant to the interpretation of experimental studies and to the possibility of reorganization of connections following injury.     

大鼠三叉神经本体觉中枢通路二级神经元中继咬肌本体觉传入的微超结构证据

将Ricin注入大鼠咬肌神经,存活2周左右,再将HRP分别定位电泳于作为三叉神经本体觉中枢通路三级传入神经元所在地的三叉神经感觉主核背内侧部(Vpdm)和三叉神经运动核腹侧区(AVM)。电镜观察结果表明,在三叉神经本体觉中枢通路二级传入神经元所在地的三叉神经脊束核吻侧亚核背内侧部(Vodm),初级传入的溃变终末与HRP逆标的树突间形成非对称型突触,确证了Vodm是三叉神经本体觉中枢通路的中继核团。突触后树突多为中间树突和近侧树突。此外,在Vodm区还发现来自Vpdm的顺行标记终末与非标记的树突形成突触。本研究证明Vodm区超微结构有以下几个特征:(1)轴-体突触极少见;(2)轴-棘突触少见;(3)突触小球结构少见;(4)大扇贝形终末较少见;(5)这一区域也有小颗粒泡和大颗粒泡终末。这些超微结构特征,可能是Vodm与三叉神经感觉核簇其它部位区别之点,也可能是本体感觉中继核团特有的结构特征。     

Ultrastructure of supraspinal dorsal root projections in the toad. II. The cerebellar granular layer

Summary Following section of the left dorsal roots, degenerating fibres and boutons were observed in the granular layer of the ipsilateral cerebellum. The degenerating terminals were identified as largeen passant varicosities of mossy fibres contacting the dendrites of presumptive granule cells. They contained round synaptic vesicles and neurofilaments and established Gray type I contacts. The terminals initially underwent filamentous degeneration with neurofilamentous hypertrophy, swollen mitochondria and loss of synaptic vesicles. At later survival times (6–30 days) they acquired an electron-dense appearance due to an increase and clumping of the filamentous component.After injection of horseradish peroxidase into the left cerebellum, all ipsilateral spinal ganglia showed a few (2–3%) labelled cells, indicating that a primary afferent contribution to this pathway originated from each segment of the spinal cord.