The innervation of the hind limb of Eleutherodactylus martinicensis: further comparison of cell and fiber numbers during development

Development ◽  
1972 ◽  
Vol 27 (2) ◽  
pp. 389-412
Author(s):  
Arthur Hughes ◽  
Margaret Egar

In montages of electron micrographs of the sciatic nerve of Eleutherodactylus martinicensis, the numbers of fibers of all classes have been counted, from the 8·5 day embryo, through the early juvenile to the adult. These counts have been compared with the total numbers of cells in the lumbar ventral horn plus those in the lumbar spinal ganglia 8, 9 and 10. In the embryo, both sets of counts rise to a peak on the 13th day, and fall early in the 14th day. In the embryo, the cell count is 600–1000 more than the fiber count, while in the 6-day juvenile onwards, the fiber count is the greater. These differences are held to arise from the play of two independent factors, namely production of axons in the embryo by only a minority of cells in ganglia and ventral horns, and secondly, the extent to which axons branch between spinal roots and sciatic nerve at all stages. In the embryo, numbers of cells and fibers maintain a parallel course up and down the 13-day peak, indicating that many cells which are lost by degeneration had already sent axons into the nerve. Myelinated fibers first appear in the limb nerves at 8·5 days, when limb motility is first seen. The course of formation of the earliest myelin in the sciatic nerve resembles that of fibers in the central nervous system. In spinal roots there are both myelinated and unmyelinated fibers, the proportion of the latter in ventral roots being the greater.

Antioxidants ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 38
Author(s):  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Bora Kim ◽  
Jae-Chul Lee ◽  
Hyun-Jin Tae ◽  
...  

Hypothermia enhances outcomes of patients after resuscitation after cardiac arrest (CA). However, the underlying mechanism is not fully understood. In this study, we investigated effects of hypothermic therapy on neuronal damage/death, microglial activation, and changes of endogenous antioxidants in the anterior horn in the lumbar spinal cord in a rat model of asphyxial CA (ACA). A total of 77 adult male Sprague–Dawley rats were randomized into five groups: normal, sham ACA plus (+) normothermia, ACA + normothermia, sham ACA + hypothermia, and ACA + hypothermia. ACA was induced for 5 min by injecting vecuronium bromide. Therapeutic hypothermia was applied after return of spontaneous circulation (ROSC) via rapid cooling with isopropyl alcohol wipes, which was maintained at 33 ± 0.5 °C for 4 h. Normothermia groups were maintained at 37 ± 0.2 °C for 4 h. Neuronal protection, microgliosis, oxidative stress, and changes of endogenous antioxidants were evaluated at 12 h, 1 day, and 2 days after ROSC following ACA. ACA resulted in neuronal damage from 12 h after ROSC and evoked obvious degeneration/loss of spinal neurons in the ventral horn at 1 day after ACA, showing motor deficit of the hind limb. In addition, ACA resulted in a gradual increase in microgliosis with time after ACA. Therapeutic hypothermia significantly reduced neuronal loss and attenuated hind limb dysfunction, showing that hypothermia significantly attenuated microgliosis. Furthermore, hypothermia significantly suppressed ACA-induced increases of superoxide anion production and 8-hydroxyguanine expression, and significantly increased superoxide dismutase 1 (SOD1), SOD2, catalase, and glutathione peroxidase. Taken together, hypothermic therapy was found to have a substantial impact on changes in ACA-induced microglia activation, oxidative stress factors, and antioxidant enzymes in the ventral horn of the lumbar spinal cord, which closely correlate with neuronal protection and neurological performance after ACA.


1967 ◽  
Vol 4 (6) ◽  
pp. 493-512
Author(s):  
V. Bergmann ◽  
C.-H. Becker

The histopathologic changes in the spinal ganglia, spinal roots, and spinal cord in 17 piglets following natural or experimental infection with the virus of pseudorabies were characterized by inflammatory mesenchymal and glial infiltrations and cellular necrosis. The lesions in the connective and vascular tissues were often more pronounced than those in neurons. Nuclear changes resembling inclusion bodies were only occasionally demonstrated. This non-specific histopathologic picture was considered to be the result of an increased resistance against the pseudorabies virus. Although the preponderantly diffuse and multicentric localization of the lesions in natural infections may point to a circulatory spread of the infection to the central nervous system, the continuity of lesions in the cord following intramuscular infection substantiates the possibility of the neuronal route of CNS infection in the pig.


1955 ◽  
Vol 102 (2) ◽  
pp. 213-236 ◽  
Author(s):  
Byron H. Waksman ◽  
Raymond D. Adams

In experimental allergic encephalomyelitis (EAE), produced by injecting rabbits with whole rabbit spinal cord together with tubercle bacilli and mineral oil, lesions comparable to those seen in the central nervous system are found in the nerve roots, spinal ganglia, and peripheral nerves. When special fractions of bovine white matter are used as antigen in rabbits, the same distribution of lesions is seen but peripheral nerve involvement is relatively less frequent. When rabbit sciatic nerve or spinal ganglia are used as antigen in rabbits, lesions occur only in the roots, ganglia, and peripheral nerves. Lesions are not produced in the central nervous system, nor is there a meningitis. This disease picture has been called experimental allergic neuritis (EAN). The antigenicity of rabbit nerve is not impaired by autoclaving. Sciatic nerve of other mammalian species produces the same disease in rabbits as does rabbit nerve. Optic nerve, used as antigen, produces the typical picture of EAE, not EAN. The optic nerves are not affected in EAN, whereas they commonly contain lesions in EAE. There are differences of symptomatology, referable to the difference in distribution of lesions, between EAE and EAN. The spinal fluid of EAE shows an increase both in the number of cells and in the total protein content. In EAN, the same changes in protein are observed, but usually the cell count remains normal. The cell count appears to be related to the involvement of cerebral and spinal meninges, which is an almost invariable accompaniment of EAE. The skin tests and serologic studies made with homologous and heterologous antigens were essentially non-contributory, apparently as a consequence of the diversity of antigens present in the inoculated materials. The similarity between EAN and certain of the human polyneuritides is indicated and discussed.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Sheng-Hua Wu ◽  
Shu-Hung Huang ◽  
Kuang-I Cheng ◽  
Chee-Yin Chai ◽  
Jwu-Lai Yeh ◽  
...  

Background. Severe burns result in hypercatabolic state and concomitant muscle atrophy that persists for several months, thereby limiting patient recovery. However, the effects of burns on the corresponding spinal dermatome remain unknown. This study aimed to investigate whether burns induce apoptosis of spinal cord ventral horn motor neurons (VHMNs) and consequently cause skeletal muscle wasting.Methods. Third-degree hindpaw burn injury with 1% total body surface area (TBSA) rats were euthanized 4 and 8 weeks after burn injury. The apoptosis profiles in the ventral horns of the lumbar spinal cords, sciatic nerves, and gastrocnemius muscles were examined. The Schwann cells in the sciatic nerve were marked with S100. The gastrocnemius muscles were harvested to measure the denervation atrophy.Result. The VHMNs apoptosis in the spinal cord was observed after inducing third-degree burns in the hindpaw. The S100 and TUNEL double-positive cells in the sciatic nerve increased significantly after the burn injury. Gastrocnemius muscle apoptosis and denervation atrophy area increased significantly after the burn injury.Conclusion. Local hindpaw burn induces apoptosis in VHMNs and Schwann cells in sciatic nerve, which causes corresponding gastrocnemius muscle denervation atrophy. Our results provided an animal model to evaluate burn-induced muscle wasting, and elucidate the underlying mechanisms.


2018 ◽  
Vol 92 (18) ◽  
Author(s):  
Jacob I. Ayers ◽  
Cara J. Riffe ◽  
Zachary A. Sorrentino ◽  
Jeffrey Diamond ◽  
Eric Fagerli ◽  
...  

ABSTRACTMisfolded alpha-synuclein (αS) may exhibit a number of characteristics similar to those of the prion protein, including the apparent ability to spread along neuroanatomical connections. The demonstration for this mechanism of spread is largely based on the intracerebral injections of preaggregated αS seeds in mice, in which it cannot be excluded that diffuse, surgical perturbations and hematogenous spread also contribute to the propagation of pathology. For this reason, we have utilized the sciatic nerve as a route of injection to force the inoculum into the lumbar spinal cord and induce a localized site for the onset of αS inclusion pathology. Our results demonstrate that mouse αS fibrils (fibs) injected unilaterally in the sciatic nerve are efficient in inducing pathology and the onset of paralytic symptoms in both the M83 and M20 lines of αS transgenic mice. In addition, a spatiotemporal study of these injections revealed a predictable spread of pathology to brain regions whose axons synapse directly on ventral motor neurons in the spinal cord, strongly supporting axonal transport as a mechanism of spread of the αS inducing, or seeding, factor. We also revealed a relatively decreased efficiency for human αS fibs containing the E46K mutation to induce disease via this injection paradigm, supportive of recent studies demonstrating a diminished ability of this mutant αS to undergo aggregate induction. These results further demonstrate prion-like properties for αS by the ability for a progression and spread of αS inclusion pathology along neuroanatomical connections.IMPORTANCEThe accumulation of alpha-synuclein (αS) inclusions is a hallmark feature of Parkinson's disease (PD) and PD-related diseases. Recently, a number of studies have demonstrated similarities between the prion protein and αS, including its ability to spread along neuroanatomical tracts throughout the central nervous system (CNS). However, there are caveats in each of these studies in which the injection routes used had the potential to result in a widespread dissemination of the αS-containing inocula, making it difficult to precisely define the mechanisms of spread. In this study, we assessed the spread of pathology following a localized induction of αS inclusions in the lumbar spinal cord following a unilateral injection in the sciatic nerve. Using this paradigm, we demonstrated the ability for αS inclusion spread and/or induction along neuroanatomical tracts within the CNS of two αS-overexpressing mouse models.


Development ◽  
1967 ◽  
Vol 17 (3) ◽  
pp. 453-471
Author(s):  
M. C. Prestige

It is the purpose of this paper to describe the development of the lumbar dorsal root ganglia after amputation of the leg. This operation can be performed at a very early stage before any connexions between the limb and the central nervous system are established. Alternatively, it can be performed at a number of later stages after the limb has been innervated. The extent of interaction can then be investigated for each stage by observing the subsequent development of the ganglia and comparing it with that of normal animals. Amputation of the limb-bud or the growing leg results in partial removal of the peripheral field for both sensory and motor neurones; the operation thus provides a means of investigating the mechanisms that control the processes of proliferation, maintenance, and degeneration of nerve cells. Detwiler and his colleagues (Detwiler, 1933) have shown that in Amblystoma loss of cells from the ganglia (hypoplasia) follows amputation, and that increase in number (hyperplasia) follows grafting of a supernumerary limb.


2019 ◽  
Vol 78 (12) ◽  
pp. 1178-1180 ◽  
Author(s):  
Suresh Mohan ◽  
Iván Coto Hernández ◽  
Martin K Selig ◽  
Shinsuke Shibata ◽  
Nate Jowett

Abstract Though unmyelinated fibers predominate axon counts within peripheral nerves, they are frequently excluded in histomorphometric assessment as they cannot be readily resolved by light microscopy. Herein, we demonstrate stain-free resolution of unmyelinated axons in Sox10-Venus mice by widefield fluorescence imaging of sciatic nerve cryosections. Optional staining of cryosections using a rapid and nontoxic myelin-specific dye (FluoroMyelin Red) enables robust synchronous resolution of myelinated and unmyelinated fibers, comprising a high-throughput platform for neural histomorphometry.


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