Artículos de revistas: "Spinal cord Axons Oligodendroglia"

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Furlan, JC, Y. Liu, W. Dietrich, MD Norenberg, S. Croul y MG Fehlings. "CNS/CSCN Chair’s Select Abstract Presentations". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (mayo de 2015): S9. http://dx.doi.org/10.1017/cjn.2015.68.

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Background: This study examines whether age is a key determinant for inflammatory response, oligodendroglial apoptosis and axonal survival after traumatic spinal cord injury (SCI). Methods: This study includes post-mortem spinal cord tissue from 64 cases of SCI (at cervical or high-thoracic level) and 38 controls cases. Each group was subdivided into younger and elderly individuals (≥65 years). Alternating sections from 2 to 3 segments caudal to SCI and age/sex/level-matched segments from controls were stained for: (i) neuroinflammation (neutrophils, macrophages, lymphocytes); (ii) apoptotic oligodendrocytes; (iii) axons; (iv) extent of degeneration. The number of cells or axons was counted in the motor and sensory areas within the spinal cord using unbiased stereological techniques. Results: Younger and elderly individuals had statistically similar number of inflammatory cells in most of the stages post-SCI. Younger and elderly individuals had similar number of oligodendrocytes in apoptosis in all stages following SCI. The number of preserved axons did not significantly differ between younger and elderly individuals with SCI and without prior CNS injury. Extend of degeneration within the spinal cord white matter did not significantly differ between the two groups. Conclusions: Our results indicate that age at the time of injury does not adversely affect the cellular inflammatory response, oligodendroglial apoptosis and axonal survival after traumatic SCI.

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Bondan, Eduardo Fernandes, Maria Anete Lallo, Maria de Fátima Monteiro Martins y Dominguita Luhers Graça. "Schwann cell expression of an oligodendrocyte-like remyelinating pattern after ethidium bromide injection in the rat spinal cord". Arquivos de Neuro-Psiquiatria 68, n.º 5 (octubre de 2010): 783–87. http://dx.doi.org/10.1590/s0004-282x2010000500021.

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Schwann cells are recognized by their capacity of producing single internodes of myelin around axons of the peripheral nervous system. In the ethidium bromide (EB) model of primary demyelination in the brainstem, it is observed the entry of Schwann cells into the central nervous system in order to contribute to the myelin repair performed by the oligodendrocytes that survived to the EB gliotoxic action, being able to even remyelinate more than one axon at the same time, in a pattern of repair similar to the oligodendroglial one. The present study was developed in the spinal cord to observe if Schwann cells maintained this competence of attending simultaneously different internodes. It was noted that, on the contrary of the brainstem, Schwann cells were the most important myelinogenic cells in the demyelinated site and, although rare, also presented the capacity of producing more than one internode of myelin in distinct axons.

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Tsata, Vasiliki, Volker Kroehne, Daniel Wehner, Fabian Rost, Christian Lange, Cornelia Hoppe, Thomas Kurth et al. "Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord". Development 147, n.º 24 (6 de noviembre de 2020): dev193946. http://dx.doi.org/10.1242/dev.193946.

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ABSTRACTSpinal cord injury (SCI) results in loss of neurons, oligodendrocytes and myelin sheaths, all of which are not efficiently restored. The scarcity of oligodendrocytes in the lesion site impairs re-myelination of spared fibres, which leaves axons denuded, impedes signal transduction and contributes to permanent functional deficits. In contrast to mammals, zebrafish can functionally regenerate the spinal cord. Yet, little is known about oligodendroglial lineage biology and re-myelination capacity after SCI in a regeneration-permissive context. Here, we report that, in adult zebrafish, SCI results in axonal, oligodendrocyte and myelin sheath loss. We find that OPCs, the oligodendrocyte progenitor cells, survive the injury, enter a reactive state, proliferate and differentiate into oligodendrocytes. Concomitantly, the oligodendrocyte population is re-established to pre-injury levels within 2 weeks. Transcriptional profiling revealed that reactive OPCs upregulate the expression of several myelination-related genes. Interestingly, global reduction of axonal tracts and partial re-myelination, relative to pre-injury levels, persist at later stages of regeneration, yet are sufficient for functional recovery. Taken together, these findings imply that, in the zebrafish spinal cord, OPCs replace lost oligodendrocytes and, thus, re-establish myelination during regeneration.

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Casha, S., W. R. Yu y M. G. Fehlings. "Oligodendroglial apoptosis occurs along degenerating axons and is associated with FAS and p75 expression following spinal cord injury in the rat". Neuroscience 103, n.º 1 (febrero de 2001): 203–18. http://dx.doi.org/10.1016/s0306-4522(00)00538-8.

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Grieb, Paweł, Maciej Świątkiewicz, Agnieszka Kamińska, Anselm Jünemann, Robert Rejdak y Konrad Rejdak. "Citicoline: A Candidate for Adjunct Treatment of Multiple Sclerosis". Pharmaceuticals 14, n.º 4 (2 de abril de 2021): 326. http://dx.doi.org/10.3390/ph14040326.

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In remitting–relapsing multiple sclerosis (RR-MS), relapses are driven by autoreactive immune cells that enter the brain and spinal cord and damage myelin sheaths of axons in white and grey matter, whereas during remissions myelin is repaired by activated oligodendroglial cells. Disease-modifying therapies (DMTs) may either retard/attenuate myelin damage or promote/enhance/speed up myelin repair. Almost all currently approved DMTs inhibit myelin damage and are considerably toxic. Enhancement of myelin repair is considered an unmet medical need of MS patients. Citicoline, known for many years as a nootropic and neuroprotective drug and recently pronounced food supplement, has been found to be significantly efficacious in two complementary rodent models of MS, experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced myelin toxicity. Moreover, citicoline treatment improves visual evoked potentials (VEPs) in glaucoma patients, which is relevant because VEP monitoring is frequently used as an indicator of remyelination in MS. Although over-the-counter availability of citicoline may impede its formal translation to the clinic of MS, evaluation of its efficacy for supporting remyelination in this disease is strongly indicated.

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Dowding, A. J. y J. Scholes. "Lymphocytes and macrophages outnumber oligodendroglia in normal fish spinal cord." Proceedings of the National Academy of Sciences 90, n.º 21 (1 de noviembre de 1993): 10183–87. http://dx.doi.org/10.1073/pnas.90.21.10183.

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Duval, Tanguy, Ariane Saliani, Harris Nami, Antonio Nanci, Nikola Stikov, Hugues Leblond y Julien Cohen-Adad. "Axons morphometry in the human spinal cord". NeuroImage 185 (enero de 2019): 119–28. http://dx.doi.org/10.1016/j.neuroimage.2018.10.033.

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Kanno, Takeshi, Tetsuro Kurotaki, Naoaki Yamada, Kotaro Yamashita, Yumi Wako y Minoru Tsuchitani. "Activity of 2′, 3′-Cyclic Nucleotide 3′-Phosphodiesterase (CNPase) in Spinal Cord with Spongy Change Induced by a Single Oral Dose of Aniline in Rats". Toxicologic Pathology 38, n.º 3 (16 de marzo de 2010): 359–65. http://dx.doi.org/10.1177/0192623310362245.

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A spongy change in the spinal cord white matter was observed in four-week-old rats treated with aniline. Although this change was found to be a result of the myelin sheath splitting at the ultrastructural level, the mechanism is unknown. This study was conducted to identify the mechanism of the spongy change in aniline-treated rats. The spongy change in the spinal cord white matter was first detected on day 5 in the histopathologic examination. The incidence and severity of the lesions, especially in the lateral and ventral funiculi of the thoracic spinal cord white matter, increased prominently from day 8 to day 10. In all rats, immunohistochemical staining by anti-2′, 3′-cyclic nucleotide 3′-phosphodiesterase (CNPase) occurred along the cytoplasmic boundaries of the normal oligodendroglia. However, mild to moderate anti-CNPase staining extended to the swollen cytoplasm of the oligodendroglia in the aniline-treated rats from day 2 to day 4. In the electron microscopic examination, free ribosomes and rough endoplasmic reticula in the cytoplasm of the oligodendroglia increased on days 3 and 4. These changes were considered to be related to CNPase expression. However, CNPase expression decreased, whereas the spongy changes were detected from day 5. The reduction in CNPase expression may contribute to the changes in the myelin morphology observed in aniline intoxication.

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Svanidze, I. K. y D. P. Museridze. "Growth of axons in organotypical spinal cord culture". Bulletin of Experimental Biology and Medicine 109, n.º 2 (febrero de 1990): 232–35. http://dx.doi.org/10.1007/bf00841682.

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10

Holley, John A. y Jerry Silver. "Growth pattern of pioneering chick spinal cord axons". Developmental Biology 123, n.º 2 (octubre de 1987): 375–88. http://dx.doi.org/10.1016/0012-1606(87)90396-4.

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Tuszynski, Mark H., Keith Murai, Armin Blesch, Ray Grill y Ian Miller. "Functional Characterization of Ngf-Secreting Cell Grafts to the Acutely Injured Spinal Cord". Cell Transplantation 6, n.º 3 (mayo de 1997): 361–68. http://dx.doi.org/10.1177/096368979700600318.

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Previously we reported that grafts of cells genetically modified to produce human nerve growth factor (hNGF) promoted specific and robust sprouting of spinal sensory, motor, and noradrenergic axons. In the present study we extend these investigations to assess NGF effects on corticospinal motor axons and on functional outcomes after spinal cord injury. Fibroblasts from adult rats were transduced to express human NGF; control cells were not genetically modified. Fibroblasts were then grafted to sites of midthoracic spinal cord dorsal hemisection lesions. Three months later, recipients of NGF-secreting grafts showed deficits on conditioned locomotion over a wire mesh that did not differ in extent from control-lesioned animals. On histological examination, NGF-secreting grafts elicited specific sprouting from spinal primary sensory afferent axons, local motor axons, and putative cerulospinal axons as previously reported, but no specific responses from corticospinal axons. Axons responding to NGF robustly penetrated the grafts but did not exit the grafts to extend to normal innervation territories distal to grafts. Grafted cells continued to express NGF protein through the experimental period of the study. These findings indicate that 1) spinal cord axons show directionally sensitive growth responses to neurotrophic factors, 2) growth of axons responding to a neurotrophic factor beyond an injury site and back to their natural target regions will likely require delivery of concentration gradients of neurotrophic factors toward the target, 3) corticospinal axons do not grow toward a cellular source of NGF, and 4) functional impairments are not improved by strictly local sprouting response of nonmotor systems.

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12

Holder, N., J. D. Clarke y D. Tonge. "Pathfinding by dorsal column axons in the spinal cord of the frog tadpole". Development 99, n.º 4 (1 de abril de 1987): 577–87. http://dx.doi.org/10.1242/dev.99.4.577.

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Sensory fibres from dorsal root ganglia (DRG) enter the spinal cord and run within a clearly defined ipsilateral pathway, the dorsal column, which lies in the dorsal funiculus. We have examined the characteristics of this pathway as a defined substrate for dorsal column axons in Rana temporaria tadpoles by rotating the thoracic spinal cord through 180 degrees from dorsal to ventral. Using HRP as a neuronal tracer we establish that many dorsal column axons from the hindlimb locate the ipsilateral or contralateral dorsal column pathway in the rotated cord. Other axons locate and grow caudally down the contralateral dorsal column returning to the lumbar region. Axons of the dorsal column never take an inappropriate pathway except at the transection sites where they negotiate abnormal routes to reach the contralateral or ipsilateral dorsal columns in normally positioned or rotated cord. The results demonstrate that the dorsal columns act as highly specific pathways for axons from DRG neurones but the axons' interactions with the pathway do not control the craniocaudal or left-right options for growth.

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Bamber, Norman I., Huaying Li, Patrick Aebischer y Xiao Ming Xu. "Fetal Spinal Cord Tissue in Mini-Guidance Channels Promotes Longitudinal Axonal Growth after Grafting into Hemisected Adult Rat Spinal Cords". Neural Plasticity 6, n.º 4 (1999): 103–21. http://dx.doi.org/10.1155/np.1999.103.

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Solid fetal spinal cord (FSC) tissue, seeded into semipermeable mini-guidance channels, was tested for the ability to promote axonal growth across the gap created by a midthoracic (T8) hemisection in adult rats. Fetal thoracic spinal cords, at embryonic days 13 to 15, were harvested and gently aspirated into mini-guidance channels (1.25 mm in diameter and 3.0 mm in length). Care was taken to maintain the rostro-caudal orientation of the FSC. In control rats, the FSC-channel congraft struct was exposed to 5 freeze/thaw cycles to produce non-viable grafts before implantation into the hemisected cord. All cases revealed intact tissue cables of various diameters spanning the rostro-caudal extent of the lesion cavity, with integration of host-graft tissues at both interfaces. Immunofluorescence results indicated that numerous neurofilament-positive axons were present within the FSC tissue cable. Double-labeling of a subpopulation of these axons with calcitonin generelated peptide indicated their peripheral nervous system (PNS) origin. Descending serotonergic and noradrenergic axons were found in the proximity of the rostral host-graft interface, but were not observed to grow into the FSC-graft. Anterograde tracing of propriospinal axons with Phaseolus vulgaris-leucoagglutinin demonstrated that axons had regenerated into the FSC-graft and had traveled longitudinally to the distal end of the channel. Few axons were observed to cross the distal host-graft interface to enter the host spinal cord. Cross-sectional analysis at the midpoint of the tissue cable stained with toluidine blue demonstrated a significant increase (P<0.01) in myelinated axons in viable FSC grafts (1455±663, mean±S.E.M.; n=6) versus freeze-thaw control grafts (155±50; n=5). In addition to the myelinated axons, many unmyelinated axons were observed in the tissue cable at the electron microscopic level. Areas resembling the PNS with typical Schwann cells, as well as those resembling the central nervous system with neurons and central neuropil, were also seen. In freeze-thaw control grafts, neither viable neurons nor central neuropil were observed. Retrograde tracing with Fast Blue and Diamidino Yellow demonstrated that neurons within the FSC graft extended axons into the host spinal cord at least for 2 mm from both the rostral and caudal host-graft interfaces. We conclude that viable FSC grafts within semipermeable guidance channels may serve both as a permissive bridge for longitudinally directed axonal growth and a potential relay for conveying information across a lesion site in the adult rat spinal cord.

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Bonnici, Brenda y Josef P. Kapfhammer. "Spontaneous regeneration of intrinsic spinal cord axons in a novel spinal cord slice culture model". European Journal of Neuroscience 27, n.º 10 (mayo de 2008): 2483–92. http://dx.doi.org/10.1111/j.1460-9568.2008.06227.x.

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Iwakawa, Masaya, Kazuo Mizoi, Alan Tessler y Yasunobu Itoh. "Intraspinal Implants of Fibrin Glue Containing Glial Cell Line-Derived Neurotrophic Factor Promote Dorsal Root Regeneration into Spinal Cord". Neurorehabilitation and Neural Repair 15, n.º 3 (septiembre de 2001): 173–82. http://dx.doi.org/10.1177/154596830101500304.

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Objective: The purpose of this study was to determine whether glial cell line—de rived neurotrophic factor (GDNF) delivered intraspinally via a fibrin glue (FG) en hanced regeneration of cut dorsal root (DR). Methods: FG containing GDNF was inserted into aspiration cavities in the lumbar enlargement of adult rats. The tran sected L5 DR stump was placed at the bottom of the cavity and sandwiched between the FG and the spinal cord. Regenerated DR axons were labeled with horseradish peroxidase (HRP) or with immunohistochemical methods for calcitonin gene-related peptide (CGRP). Results: Primary afferent axons labeled with HRP regenerated into the spinal cord, received GDNF, and made frequent arborization there. Some of these were myelinated axons that established synapses on intraspinal neuronal profiles. CGRP-immunoreactive DR axons extended into the motor neurons and formed promi nent varicosities around their cell bodies. Only a few axons regenerated into the spinal cords given FG without GONE Conclusions: Our results indicate that GDNF en hances regeneration of DR into the adult rat spinal cord and that GDNF may be ef fectively supplied to the intraspinal injury site via FG. Because the regenerated axons establish synapses on intraspinal neurons, this therapeutic strategy has the potential to help to rebuild spinal reflex circuits interrupted by spinal cord injury. Key Words: GDNF—Fibrin glue—Intraspinal injury—Calcitonin gene-related peptide—Dorsal root regeneration—Electron microscopy—Glial cell line-derived neurotrophic fac tor—Horseradish peroxidase.

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Pallini, Roberto, Eduardo Fernandez, Carlo Gangitano, Aurora Del Fà, Corrado Olivieri-Sangiacomo y Alessandro Sbriccoli. "Studies on embryonic transplants to the transected spinal cord of adult rats". Journal of Neurosurgery 70, n.º 3 (marzo de 1989): 454–62. http://dx.doi.org/10.3171/jns.1989.70.3.0454.

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✓ Spinal cord tissue was obtained from 13- and 14-day embryonic rats and homologously grafted to the completely transected spinal cord of adult rats. Eight and 12 weeks after grafting, clinical, electrophysiological, histological, and neuroanatomical studies were performed. Motor performance of the hosts was assessed by the inclined-plane test. The conduction of nerve impulses across the lesion-transplantation site was evaluated by recording the spinal corticomotor and somatosensory evoked potentials. The survival, growth, differentiation, and parenchymal integration of the graft were documented histologically on semi-thin sections. The axonal interactions between the host spinal cord and the graft as well as the posttraumatic retrograde degeneration of corticospinal axons were investigated using the horseradish peroxidase (HRP) technique. Clinical and electrophysiological assessments did not demonstrate any functional activity of the graft. On histological examination, grafted neurons showed a survival rate of 55%. Such neurons exhibited a limited degree of growth and differentiation. The extent of parenchymal integration between the host spinal cord and the graft varied considerably among different specimens and in the various regions of every specimen. The HRP investigations demonstrated that some axonal interactions between the host spinal cord and the graft had occurred. Regenerated axons arising from both the spinal cord and the dorsal root ganglia of the host entered the graft and elongated in it. Also, axons from the grafted neurons were able to grow for some distance in the host spinal cord. The phenomenon of the posttraumatic retrograde degeneration of corticospinal axons was not affected by this embryonic tissue grafting.

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17

Dickson, Barry J. "Wnts send axons up and down the spinal cord". Nature Neuroscience 8, n.º 9 (septiembre de 2005): 1130–32. http://dx.doi.org/10.1038/nn0905-1130.

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Radojicic, Milan, Paul J. Reier, Oswald Steward y Hans S. Keirstead. "Septations in chronic spinal cord injury cavities contain axons". Experimental Neurology 196, n.º 2 (diciembre de 2005): 339–41. http://dx.doi.org/10.1016/j.expneurol.2005.08.009.

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Blight, A. R. y S. Someya. "Depolarizing afterpotentials in myelinated axons of mammalian spinal cord". Neuroscience 15, n.º 1 (mayo de 1985): 1–12. http://dx.doi.org/10.1016/0306-4522(85)90118-6.

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20

Imondi, Ralph y Zaven Kaprielian. "Commissural axon pathfinding on the contralateral side of the floor plate: a role for B-class ephrins in specifying the dorsoventral position of longitudinally projecting commissural axons". Development 128, n.º 23 (1 de diciembre de 2001): 4859–71. http://dx.doi.org/10.1242/dev.128.23.4859.

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In both invertebrate and lower vertebrate species, decussated commissural axons travel away from the midline and assume positions within distinct longitudinal tracts. We demonstrate that in the developing chick and mouse spinal cord, most dorsally situated commissural neuron populations extend axons across the ventral midline and through the ventral white matter along an arcuate trajectory on the contralateral side of the floor plate. Within the dorsal (chick) and intermediate (mouse) marginal zone, commissural axons turn at a conserved boundary of transmembrane ephrin expression, adjacent to which they form a discrete ascending fiber tract. In vitro perturbation of endogenous EphB-ephrinB interactions results in the failure of commissural axons to turn at the appropriate dorsoventral position on the contralateral side of the spinal cord; consequently, axons inappropriately invade more dorsal regions of B-class ephrin expression in the dorsal spinal cord. Taken together, these observations suggest that B-class ephrins act locally during a late phase of commissural axon pathfinding to specify the dorsoventral position at which decussated commissural axons turn into the longitudinal axis.

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Papasozomenos, S. C., L. I. Binder, P. K. Bender y M. R. Payne. "Microtubule-associated protein 2 within axons of spinal motor neurons: associations with microtubules and neurofilaments in normal and beta,beta'-iminodipropionitrile-treated axons." Journal of Cell Biology 100, n.º 1 (1 de enero de 1985): 74–85. http://dx.doi.org/10.1083/jcb.100.1.74.

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We have examined the distribution of microtubule-associated protein 2 (MAP2) in the lumbar segment of spinal cord, ventral and dorsal roots, and dorsal root ganglia of control and beta,beta'-iminodipropionitrile-treated rats. The peroxidase-antiperoxidase technique was used for light and electron microscopic immunohistochemical studies with two monoclonal antibodies directed against different epitopes of Chinese hamster brain MAP2, designated AP9 and AP13. MAP2 immunoreactivity was present in axons of spinal motor neurons, but was not detected in axons of white matter tracts of spinal cord and in the majority of axons of the dorsal root. A gradient of staining intensity among dendrites, cell bodies, and axons of spinal motor neurons was present, with dendrites staining most intensely and axons the least. While dendrites and cell bodies of all neurons in the spinal cord were intensely positive, neurons of the dorsal root ganglia were variably stained. The axons of labeled dorsal root ganglion cells were intensely labeled up to their bifurcation; beyond this point, while only occasional central processes in dorsal roots were weakly stained, the majority of peripheral processes in spinal nerves were positive. beta,beta'-Iminodipropionitrile produced segregation of microtubules and membranous organelles from neurofilaments in the peripheral nervous system portion and accumulation of neurofilaments in the central nervous system portion of spinal motor axons. While both anti-MAP2 hybridoma antibodies co-localized with microtubules in the central nervous system portion, only one co-localized with microtubules in the peripheral nervous system portion of spinal motor axons, while the other antibody co-localized with neurofilaments and did not stain the central region of the axon which contained microtubules. These findings suggest that (a) MAP2 is present in axons of spinal motor neurons, albeit in a lower concentration or in a different form than is present in dendrites, and (b) the MAP2 in axons interacts with both microtubules and neurofilaments.

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Houle, John D. y Mei Kheng Ziegler. "Bridging a Complete Transection Lesion of Adult Rat Spinal Cord with Growth Factor-Treated Nitrocellulose Implants". Journal of Neural Transplantation and Plasticity 5, n.º 2 (1994): 115–24. http://dx.doi.org/10.1155/np.1994.115.

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The ability of a substrate bound neurotrophic factor to promote growth of ascending sensory axons across a complete transection lesion of the rat spinal cord was examined in a transplantation model. Aspiration lesions created a 3 mm long cavity in the upper lumbar spinal cord of adult rats. Five weeks after injury two strips of nerve growth factortreated nitrocellulose, were implanted, each in a medio-lateral position, and apposed to the rostral and caudal surfaces of the cavity. Control animals received untreated nitrocellulose implants. Fetal spinal cord tissue was transplanted alongsideand between these strips. Six weeks post transplantation, animals were sacrificed and vibratome sections through the grafts were processed for immunocytochemical demonstration of ingrowing axons expressing calcitonin gene-related peptide (CGRP-IR), Immunolabeled axons were abundant at the caudal interface between host tissue and the NGF-treated nitrocellulose implants, with dense fascicles of fibers abutting the grafts. As the distance from the caudal surface increased some CGRP-IR fibers extended into the fetal tissue although most appeared to remain oriented in a longitudinal course adjacent to the nitrocellulose. Labeled axons were evident along the entire length of the nitrocellulose and appeared to aggregate at the rostral tip of the implant, with many fibers extending into the host spinal cord rostral to the lesion/transplant site. When untreated nitrocellulose was implanted, fewer labeled axons appeared to extend beyond the caudal host-graft interface. Most CGRP-IR axons displayed limited association or contact with the untreated nitrocellulose in this condition. Computer-assisted quantitative analysis indicated that NGF-treated nitrocellulose supported regrowing host axons for nearly three times the length exhibited by axons associated with non-treated nitrocellulose implants. These results indicate that substrate bound nerve growth factor has the capacity to enhance the regrowth of ascending sensory axons across a traumatic spinal cord injury site. The potential to reestablish functional contacts across such a lesion may be heightened by the ability of neurotrophic factors to promote more extensive axonal regrowth.

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Sinha, Kusum, Soheila Karimi-Abdolrezaee, Alexander A. Velumian y Michael G. Fehlings. "Functional Changes in Genetically Dysmyelinated Spinal Cord Axons of Shiverer Mice: Role of Juxtaparanodal Kv1 Family K+ Channels". Journal of Neurophysiology 95, n.º 3 (marzo de 2006): 1683–95. http://dx.doi.org/10.1152/jn.00899.2005.

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Axonal dysfunction after spinal cord injury (SCI) and other types of neurotrauma is associated with demyelination and exposure of juxtaparanodal K+ channels. In this study, sucrose gap electrophysiology using selective and nonselective K+ channel blockers, confocal immunohistochemistry, and Western blotting were used to study the role of Kv1.1 and Kv1.2 K+ channel subunits in dysmyelination-induced spinal cord axonal dysfunction in s hiverer mice, which lack the gene encoding myelin basic protein (MBP) and exhibit incomplete myelin sheath formation on CNS axons. The s hiverer spinal cord axons exhibited smaller amplitude of compound action potentials (CAPs), reduced conduction velocity, reduced excitability, and greater degree of high-frequency conduction failure. The “fast” K+ channel blocker 4-aminopyridine, the toxin DTX-I, which targets the Kv1.1 and Kv1.2, but not DTX- K, which has higher selectivity for Kv1.1, increased the amplitude and area of CAPs of shiverer mice spinal cord axons but had insignificant effects in wild-type mice. Confocal immunohistochemistry showed that, unlike wild-type mice, which have a precise juxtaparanodal localization of the Kv1.l and Kv1.2 K+ channel subunits, shiverer mouse axons displayed a dispersed distribution of these subunits along the internodes. In contrast, the Kv1.l and Kv1.2 subunits, Na+ channels remained highly localized to the nodal regions. Western blotting showed an increased expression of Kv 1.1 and 1.2 in the shiverer mouse spinal cord. These results provide evidence that the neurological deficits associated with myelin deficiency reflect the altered distribution and expression of the K+ channel subunits Kv1.l and Kv1.2 along the internodes of spinal cord axons associated with the biophysical consequences caused by alterations in the myelin sheaths.

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Bannerman, Peter, Ashleigh Hahn, Athena Soulika, Vittorio Gallo y David Pleasure. "Astrogliosis in EAE spinal cord: Derivation from radial glia, and relationships to oligodendroglia". Glia 55, n.º 1 (2006): 57–64. http://dx.doi.org/10.1002/glia.20437.

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Lo, Albert C., Carl Y. Saab, Joel A. Black y Stephen G. Waxman. "Phenytoin Protects Spinal Cord Axons and Preserves Axonal Conduction and Neurological Function in a Model of Neuroinflammation In Vivo". Journal of Neurophysiology 90, n.º 5 (noviembre de 2003): 3566–71. http://dx.doi.org/10.1152/jn.00434.2003.

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Axonal degeneration within the spinal cord contributes substantially to neurological disability in multiple sclerosis (MS). Thus neuroprotective therapies that preserve axons, so that they maintain their integrity and continue to function, might be expected to result in improved neurological outcome. Sodium channels are known to provide a route for sodium influx that can drive calcium influx, via reverse operation of the Na+/Ca2+ exchanger, after injury to axons within the CNS, and sodium channel blockers have been shown to protect CNS axons from degeneration after experimental anoxic, traumatic, and nitric oxide (NO)-induced injury. In this study, we asked whether phenytoin, which is known to block sodium channels, can protect spinal cord axons from degeneration in mice with experimental allergic encephalomyelitis (EAE), which display substantial axonal degeneration and clinical paralysis. We demonstrate that the loss of dorsal corticospinal tract (63%) and dorsal column (cuneate fasciculus; 43%) axons in EAE is significantly ameliorated (corticospinal tract: 28%; cuneate fasciculus: 17%) by treatment with phenytoin. Spinal cord compound action potentials (CAP) were significantly attenuated in untreated EAE, whereas spinal cords from phenytoin-treated EAE had robust CAPs, similar to those from phenytoin-treated control mice. Clinical scores in phenytoin-treated EAE at 28 days were significantly improved (1.5, i.e., minor righting reflex abnormalities) compared with untreated EAE (3.8, i.e., near-complete hindlimb paralysis). Our results demonstrate that phenytoin has a protective effect in vivo on spinal cord axons, preventing their degeneration, maintaining their ability to conduct action potentials, and improving clinical status in a model of neuroinflammation.

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Bovolenta, P. y J. Dodd. "Perturbation of neuronal differentiation and axon guidance in the spinal cord of mouse embryos lacking a floor plate: analysis of Danforth's short-tail mutation". Development 113, n.º 2 (1 de octubre de 1991): 625–39. http://dx.doi.org/10.1242/dev.113.2.625.

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The floor plate of the vertebrate nervous system has been implicated in the guidance of commissural axons at the ventral midline. Experiments in chick have also suggested that at earlier stages of development the floor plate induces the differentiation of motor neurons and other neurons of the ventral spinal cord. Here we have examined the development of the spinal cord in a mouse mutant, Danforth's short-tail, in which the floor plate is absent from caudal regions of the neuraxis. In affected regions of the spinal cord, commissural axons exhibited aberrant projection patterns as they reached and crossed the ventral midline. In addition, motor neurons were absent or markedly reduced in number in regions of the spinal cord lacking a floor plate. Our results suggest that the floor plate is indeed an intermediate target in the projection of commissural axons and support the idea that several different mechanisms operate in concert in the guidance of axons to their cellular targets in the developing nervous system. In addition, these experiments suggest that the mechanisms that govern the differentiation of the floor plate and other ventral cell types in the neural tube are common to mammals and lower vertebrates.

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27

Saywell, S. A., T. W. Ford, C. F. Meehan, A. J. Todd y P. A. Kirkwood. "Electrophysiological and Morphological Characterization of Propriospinal Interneurons in the Thoracic Spinal Cord". Journal of Neurophysiology 105, n.º 2 (febrero de 2011): 806–26. http://dx.doi.org/10.1152/jn.00738.2010.

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Propriospinal interneurons in the thoracic spinal cord have vital roles not only in controlling respiratory and trunk muscles, but also in providing possible substrates for recovery from spinal cord injury. Intracellular recordings were made from such interneurons in anesthetized cats under neuromuscular blockade and with the respiratory drive stimulated by inhaled CO2. The majority of the interneurons were shown by antidromic activation to have axons descending for at least two to four segments, mostly contralateral to the soma. In all, 81% of the neurons showed postsynaptic potentials (PSPs) to stimulation of intercostal or dorsal ramus nerves of the same segment for low-threshold (≤5T) afferents. A monosynaptic component was present for the majority of the peripherally evoked excitatory PSPs. A central respiratory drive potential was present in most of the recordings, usually of small amplitude. Neurons depolarized in either inspiration or expiration, sometimes variably. The morphology of 17 of the interneurons and/or of their axons was studied following intracellular injection of Neurobiotin; 14 axons were descending, 6 with an additional ascending branch, and 3 were ascending (perhaps actually representing ascending tract cells); 15 axons were crossed, 2 ipsilateral, none bilateral. Collaterals were identified for 13 axons, showing exclusively unilateral projections. The collaterals were widely spaced and their terminations showed a variety of restricted locations in the ventral horn or intermediate area. Despite heterogeneity in detail, both physiological and morphological, which suggests heterogeneity of function, the projections mostly fitted a consistent general pattern: crossed axons, with locally weak, but widely distributed terminations.

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28

Shifman, M. I. y M. E. Selzer. "Expression of the Netrin Receptor UNC-5 in Lamprey Brain: Modulation by Spinal Cord Transection". Neurorehabilitation and Neural Repair 14, n.º 1 (marzo de 2000): 49–58. http://dx.doi.org/10.1177/154596830001400106.

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The sea lamprey recovers from spinal cord transection by a process that involves directionally specific regeneration of axons. The mechanisms underlying this speci ficity are not known, but they may involve molecular cues similar to those that guide the growth of spinal cord axons during development, such as netrins and semaphorins. To test the role of guidance cues in regeneration, we cloned netrin and its receptor UNC-5 from lamprey central nervous system (CNS) and studied their expression after spinal cord transection. In situ hybridization showed that (1) mRNA for netrin is ex pressed in the spinal cord, primarily in neurons of the lateral gray matter and in dor sal cells; (2) mRNA for UNC-5 is expressed in lamprey reticulospinal neurons; (3) fol lowing spinal cord transection, UNC-5 message was dramatically downregulated at two weeks, during the period of axon dieback; (4) UNC-5 message was upregulated at three weeks, when many axons are beginning to regenerate; and (5) axotomy-in duced expression of UNC-5 occurred primarily in neurons whose axons regenerate poorly. Because the UNC-5 receptor is thought to mediate the chemorepellent ef fects of netrins, netrin signaling may play a role in limiting or channeling the regen eration of certain neurons. These data strengthen the rationale for studying the role of developmental guidance molecules in CNS regeneration.

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29

Kakulas, Byron A. "Spinal Cord Injuries the Facts of Neuropathology: Opportunities and Limitations". Current Neuropsychiatry and Clinical Neuroscience Reports 1, n.º 1 (4 de julio de 2019): 1–5. http://dx.doi.org/10.33702/cncnr.2019.1.1.1.

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It is essential for research projects which are undertaken to find a “cure” for human spinal cord injury (SCI) to be consistent with the neuropathological facts of the disorder. In this respect there are three main points to be taken into account. Firstly, the researcher should be aware that simple transection of the spinal cord is not a feature of human SCI. The usual lesion is one of compression and disruption with haemorrhage. The second and most important aspect of human SCI is to understand that Wallerian degeneration inevitably ensues following disruption of the axon. Wallerian degeneration is progressive and inexorable and unlike the peripheral nervous system CNS axons do not regenerate. The third and more helpful fact is that in the majority (71%) of SCI autopsies a small amount of white matter, myelin and axons, was found to be preserved at the level of injury. Re-activation of these dormant, axons offers the opportunity for improvement of the SCI patient’s neurological status by means of restorative neurology (RN).

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30

Pallini, Roberto, Eduardo Fernandez y Alessandro Sbriccoli. "Retrograde degeneration of corticospinal axons following transection of the spinal cord in rats". Journal of Neurosurgery 68, n.º 1 (enero de 1988): 124–28. http://dx.doi.org/10.3171/jns.1988.68.1.0124.

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✓ The extent of the retrograde degeneration of corticospinal axons following transection of the spinal cord was studied in rats by labeling corticospinal axons with anterogradely transported horseradish peroxidase injected in the sensorimotor cortex. Axotomized corticospinal axons underwent progressive and continuing retrograde degeneration. In specimens examined 5, 14, 28, and 56 days after trauma, the tips of the transected corticospinal axons were seen to terminate at 181 ± 80 µm, 977 ± 203 µm, 1751 ± 344 µm, and 2559 ± 466 µm (mean ± standard deviation), respectively, from the site of transection. The rate of retrograde degeneration varied according to the interval after spinal cord transection, as follows: 36.2 µm/day during the first 5 days; 88.4 µm/day between 5 and 14 days; 55.3 µm/day between 14 and 28 days; and 28.8 µm/day between 28 and 56 days. These findings may serve as useful parameters for the objective assessment of therapeutic modalities in spinal cord injury research.

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31

Bartolomei, Juan C. y Charles A. Greer. "Olfactory Ensheathing Cells: Bridging the Gap in Spinal Cord Injury". Neurosurgery 47, n.º 5 (1 de noviembre de 2000): 1057–69. http://dx.doi.org/10.1097/00006123-200011000-00006.

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Abstract SPINAL CORD INJURY (SCI) continues to be an insidious and challenging problem for scientists and clinicians. Recent neuroscientific advances have changed the pessimistic notion that axons are not capable of significant extension after transection. The challenges of recovering from SCI have been broadly divided into four areas: 1) cell survival; 2) axon regeneration (growth); 3) correct targeting by growing axons; and 4) establishment of correct and functional synaptic appositions. After acute SCI, there seems to be a therapeutic window of opportunity within which the devastating consequences of the secondary injury can be ameliorated. This is supported by several observations in which apoptotic glial cells have been identified up to 1 week after acute SCI. Moreover, autopsy studies have identified anatomically preserved but unmyelinated axons that could potentially subserve normal physiological properties. These observations suggest that therapeutic strategies after SCI can be directed into two broad modalities: 1) prevention or amelioration of the secondary injury, and 2) restorative or regenerative interventions. Intraspinal transplants have been used after SCI as a means for restoring the severed neuraxis. Fetal cell transplants and, more recently, progenitor cells have been used to restore intraspinal circuitry or to serve as relay for damaged axons. In an attempt to remyelinate anatomically preserved but physiologically disrupted axons, newer therapeutic interventions have incorporated the transplantation of myelinating cells, such as Schwann cells, oligodendrocytes, and olfactory ensheathing cells. Of these cells, the olfactory ensheathing cells have become a more favorable candidate for extensive remyelination and axonal regeneration. Olfactory ensheathing cells are found along the full length of the olfactory nerve, from the basal lamina of the epithelium to the olfactory bulb, crossing the peripheral nervous system-central nervous system junction. In vitro, these cells promote robust axonal growth, in part through cell adhesion molecules and possibly by secretion of neurotrophic growth factors that support axonal elongation and extension. In animal models of SCI, transplantation of ensheathing cells supports axonal remyelination and extensive migration throughout the length of the spinal cord. Although the specific properties of these cells that govern enhanced axon regeneration remain to be elucidated, it seems certain that they will contribute to the establishment of new horizons in SCI research.

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32

Li, Qun, Thierry Houdayer, Su Liu y Visar Belegu. "Induced Neural Activity Promotes an Oligodendroglia Regenerative Response in the Injured Spinal Cord and Improves Motor Function after Spinal Cord Injury". Journal of Neurotrauma 34, n.º 24 (15 de diciembre de 2017): 3351–61. http://dx.doi.org/10.1089/neu.2016.4913.

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33

LoPachin, Richard M., Christopher L. Gaughan, Ellen J. Lehning, Yoshiro Kaneko, Thomas M. Kelly y Andrew Blight. "Experimental Spinal Cord Injury: Spatiotemporal Characterization of Elemental Concentrations and Water Contents in Axons and Neuroglia". Journal of Neurophysiology 82, n.º 5 (1 de noviembre de 1999): 2143–53. http://dx.doi.org/10.1152/jn.1999.82.5.2143.

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To examine the role of axonal ion deregulation in acute spinal cord injury (SCI), white matter strips from guinea pig spinal cord were incubated in vitro and were subjected to graded focal compression injury. At several postinjury times, spinal segments were removed from incubation and rapidly frozen. X-ray microanalysis was used to measure percent water and dry weight elemental concentrations (mmol/kg) of Na, P, Cl, K, Ca, and Mg in selected morphological compartments of myelinated axons and neuroglia from spinal cord cryosections. As an index of axon function, compound action potentials (CAP) were measured before compression and at several times thereafter. Axons and mitochondria in epicenter of severely compressed spinal segments exhibited early (5 min) increases in mean Na and decreases in K and Mg concentrations. These elemental changes were correlated to a significant reduction in CAP amplitude. At later postcompression times (15 and 60 min), elemental changes progressed and were accompanied by alterations in compartmental water content and increases in mean Ca. Swollen axons were evident at all postinjury times and were characterized by marked element and water deregulation. Neuroglia and myelin in severely injured epicenter also exhibited significant disruptions. In shoulder areas (adjacent to epicenter) of severely injured spinal strips, axons and mitochondria exhibited modest increases in mean Na in conjunction with decreases in K, Mg, and water content. Following moderate compression injury to spinal strips, epicenter axons exhibited early (10 min postinjury) element and water deregulation that eventually recovered to near control values (60 min postinjury). Na+ channel blockade by tetrodotoxin (TTX, 1 μM) perfusion initiated 5 min after severe crush diminished both K loss and the accumulation of Na, Cl, and Ca in epicenter axons and neuroglia, whereas in shoulder regions TTX perfusion completely prevented subcellular elemental deregulation. TTX perfusion also reduced Na entry in swollen axons but did not affect K loss or Ca gain. Thus graded compression injury of spinal cord produced subcellular elemental deregulation in axons and neuroglia that correlated with the onset of impaired electrophysiological function and neuropathological alterations. This suggests that the mechanism of acute SCI-induced structural and functional deficits are mediated by disruption of subcellular ion distribution. The ability of TTX to reduce elemental deregulation in compression-injured axons and neuroglia implicates a significant pathophysiological role for Na+ influx in SCI and suggests Na+ channel blockade as a pharmacotherapeutic strategy.

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34

Saueressig, H., J. Burrill y M. Goulding. "Engrailed-1 and netrin-1 regulate axon pathfinding by association interneurons that project to motor neurons". Development 126, n.º 19 (1 de octubre de 1999): 4201–12. http://dx.doi.org/10.1242/dev.126.19.4201.

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During early development, multiple classes of interneurons are generated in the spinal cord including association interneurons that synapse with motor neurons and regulate their activity. Very little is known about the molecular mechanisms that generate these interneuron cell types, nor is it known how axons from association interneurons are guided toward somatic motor neurons. By targeting the axonal reporter gene τ-lacZ to the En1 locus, we show the cell-type-specific transcription factor Engrailed-1 (EN1) defines a population of association neurons that project locally to somatic motor neurons. These EN1 interneurons are born early and their axons pioneer an ipsilateral longitudinal projection in the ventral spinal cord. The EN1 interneurons extend axons in a stereotypic manner, first ventrally, then rostrally for one to two segments where their axons terminate close to motor neurons. We show that the growth of EN1 axons along a ventrolateral pathway toward motor neurons is dependent on netrin-1 signaling. In addition, we demonstrate that En1 regulates pathfinding and fasciculation during the second phase of EN1 axon growth in the ventrolateral funiculus (VLF); however, En1 is not required for the early specification of ventral interneuron cell types in the embryonic spinal cord.

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35

He, Miao, Yuetong Ding, Chen Chu, Jing Tang, Qi Xiao y Zhen-Ge Luo. "Autophagy induction stabilizes microtubules and promotes axon regeneration after spinal cord injury". Proceedings of the National Academy of Sciences 113, n.º 40 (16 de septiembre de 2016): 11324–29. http://dx.doi.org/10.1073/pnas.1611282113.

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Remodeling of cytoskeleton structures, such as microtubule assembly, is believed to be crucial for growth cone initiation and regrowth of injured axons. Autophagy plays important roles in maintaining cellular homoeostasis, and its dysfunction causes neuronal degeneration. The role of autophagy in axon regeneration after injury remains speculative. Here we demonstrate a role of autophagy in regulating microtubule dynamics and axon regeneration. We found that autophagy induction promoted neurite outgrowth, attenuated the inhibitory effects of nonpermissive substrate myelin, and decreased the formation of retraction bulbs following axonal injury in cultured cortical neurons. Interestingly, autophagy induction stabilized microtubules by degrading SCG10, a microtubule disassembly protein in neurons. In mice with spinal cord injury, local administration of a specific autophagy-inducing peptide, Tat-beclin1, to lesion sites markedly attenuated axonal retraction of spinal dorsal column axons and cortical spinal tract and promoted regeneration of descending axons following long-term observation. Finally, administration of Tat-beclin1 improved the recovery of motor behaviors of injured mice. These results show a promising effect of an autophagy-inducing reagent on injured axons, providing direct evidence supporting a beneficial role of autophagy in axon regeneration.

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36

Shi, Riyi, Tomoko Asano, Neil C. Vining y Andrew R. Blight. "Control of Membrane Sealing in Injured Mammalian Spinal Cord Axons". Journal of Neurophysiology 84, n.º 4 (1 de octubre de 2000): 1763–69. http://dx.doi.org/10.1152/jn.2000.84.4.1763.

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The process of sealing of damaged axons was examined in isolated strips of white matter from guinea pig spinal cord by recording the “compound membrane potential,” using a sucrose-gap technique, and by examining uptake of horseradish peroxidase (HRP). Following axonal transection, exponential recovery of membrane potential occurred with a time constant of 20 ± 5 min, at 37°C, and extracellular calcium activity ([Ca2+]o) of 2 mM. Most axons excluded HRP by 30 min following transection. The rate of sealing was reduced by lowering calcium and was effectively blocked at [Ca2+]o ≤ 0.5 mM, under which condition most axons continued to take up HRP for more than 1 h. Sealing at higher [Ca2+]o was blocked by calpain inhibitors (calpeptin and calpain inhibitor-1) indicating a requirement for type II (mM) calpain in the sealing process. Following compression injury, the amplitude of the maximal compound action potential conducted through the injury site was reduced. The extent of amplitude reduction was increased when the tract was superfused with calcium-free Krebs' solution (Ca2+ replaced by Mg2+). These results suggest that the fall in [Ca2+]o seen following injury in vivo is sufficient to prevent membrane sealing and may paradoxically contribute to axonal dieback, retrograde cell death, and “secondary” axonal disruption.

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37

Yaginuma, H., T. Shiga, S. Homma, R. Ishihara y R. W. Oppenheim. "Identification of early developing axon projections from spinal interneurons in the chick embryo with a neuron specific beta-tubulin antibody: evidence for a new ‘pioneer’ pathway in the spinal cord". Development 108, n.º 4 (1 de abril de 1990): 705–16. http://dx.doi.org/10.1242/dev.108.4.705.

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The early development of interneurons in the chick embryo spinal cord was studied using a monoclonal antibody against a neuron-specific beta-tubulin isoform. Early developing interneurons were divided into two cell groups on the basis of their location and the pattern of growth of their axons. One group is composed of cells that establish a primitive longitudinal pathway (PL-cells), whereas the other group contains cells constituting a circumferential pathway (C-cells). The onset of axonal development in both cell groups occurs at stage (st.) 15 (embryonic day, (E), 2) in the branchial segments, which is prior to axonogenesis of motoneurons. PL-cells develop in the region between the floor plate and the motoneuron nucleus. Their axons are the first neuronal processes (‘pioneer axons’) to arrive in the ventrolateral marginal zone and they project both rostrally and caudally to establish a primitive longitudinal association pathway at the ventrolateral surface of the neural tube. This pathway is formed before axons of C-cells arrive in the ventrolateral region. The first C-cells are initially located in the most dorsal portion of the neural tube, whereas later appearing C-cells are also located in both intermediate and ventral regions of the neural tube. The axons of C-cells project ventrally, without fasciculating, along the lateral border of the neural tube. Some of their axons enter the ipsilateral ventrolateral longitudinal pathway at st. 17. We often observed apparent contacts and interactions between preexisting axons of PL-cells and newly arriving axons of C-cells. The axons of commissural C-cells first enter the floor plate at st. 17 and cross the midline at st. 18. Axons of C cells begin to join the contralateral ventrolateral longitudinal pathway at st. 18+ to st. 19. In the floor plate region, contacts between growth cones and axons were often observed. However, axons in the floor plate at these stages were not fasciculated. These observations establish the timing and pattern of growth of axons from two specific populations of early developing interneurons in the chick spinal cord. Additionally, we have identified an early and apparently previously undescribed ‘pioneer’ pathway that constitutes the first longitudinal pathway in the chick spinal cord.

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38

CARLSTEDT, T. "Experimental Studies on Surgical Treatment of Avulsed Spinal Nerve Roots in Brachial Plexus Injury". Journal of Hand Surgery 16, n.º 5 (octubre de 1991): 477–82. http://dx.doi.org/10.1016/0266-7681(91)90098-9.

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This review summarises studies aiming at a surgical treatment of spinal nerve root avulsions from the spinal cord in brachial plexus lesions. After dorsal root injury, regrowth of nerve fibres into the spinal cord occurs only in the immature animal. After ventral root avulsion and subsequent implantation into the spinal cord, neuroanatomical and neurophysiological data show that motoneurons are capable of producing new axons which enter the implanted root. Intra-neuronal physiological experiments demonstrate that new axons can conduct action potentials and elicit muscle responses. The neurons are reconnected in segmental spinal cord activity and respond to impulses in sensory nerve fibres. In primate experiments, implantation of avulsed ventral roots in the brachial plexus resulted in functional restitution. These studies indicate the possibility of surgical treatment of ventral root avulsion injuries in brachial plexus lesions in humans.

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39

Yamada, Hajime, Toshihiko Miyake y Tadahisa Kitamura. "Regeneration of Axons in Transection of the Carp Spinal Cord". Zoological Science 12, n.º 3 (junio de 1995): 325–32. http://dx.doi.org/10.2108/zsj.12.325.

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40

DePaoli, Damon, Alicja Gasecka, Mohamed Bahdine, Jean M. Deschenes, Laurent Goetz, Jimena Perez-Sanchez, Robert P. Bonin, Yves De Koninck, Martin Parent y Daniel C. Côté. "Anisotropic light scattering from myelinated axons in the spinal cord". Neurophotonics 7, n.º 01 (10 de marzo de 2020): 1. http://dx.doi.org/10.1117/1.nph.7.1.015011.

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41

Ramer, Matt S., John V. Priestley y Stephen B. McMahon. "Functional regeneration of sensory axons into the adult spinal cord". Nature 403, n.º 6767 (enero de 2000): 312–16. http://dx.doi.org/10.1038/35002084.

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42

Roush, W. "NEUROSCIENCE: Are Pushy Axons a Key to Spinal Cord Repair?" Science 276, n.º 5321 (27 de junio de 1997): 1971–72. http://dx.doi.org/10.1126/science.276.5321.1971.

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43

Harvey, P., B. Gong, A. J. Rossomando y E. Frank. "Topographically specific regeneration of sensory axons in the spinal cord". Proceedings of the National Academy of Sciences 107, n.º 25 (4 de junio de 2010): 11585–90. http://dx.doi.org/10.1073/pnas.1003287107.

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44

Schwab, M. E. y D. Bartholdi. "Degeneration and regeneration of axons in the lesioned spinal cord". Physiological Reviews 76, n.º 2 (1 de abril de 1996): 319–70. http://dx.doi.org/10.1152/physrev.1996.76.2.319.

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For many decades, the inability of lesioned central neurons to regrow was accepted almost as a "law of nature", and on the clinical level, spinal cord and brain lesions were seen as being irreversible. Today we are starting to understand the mechanisms of neuronal regeneration in the central nervous system and its presence in the periphery. There is now a rapid expansion in this field of neuroscience. Developmental neurobiology has produced tools and concepts that start to show their impact on regeneration research. This is particularly true for the availability of antibodies and factors and for the rapidly growing cellular and molecular understanding of crucial aspects of neurite growth, guidance, target finding, and synapse stabilization. New cell biological concepts on the mechanisms of neuron survival and death and on the interaction of inflammatory cells with the central nervous system also find their way into the field of spinal cord and brain lesions and have, indeed, led already to new therapeutic approaches. This review briefly summarizes the current knowledge on the mechanisms involved in degeneration and tissue loss and in axonal regeneration subsequent to spinal cord lesions, particularly in mammals and humans.

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45

Nagashima, Masabumi y Yoshiro Inoue. "Postnatal development of corticospinal axons in the rat spinal cord". Neuroscience Research Supplements 17 (enero de 1992): 181. http://dx.doi.org/10.1016/0921-8696(92)91018-2.

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46

Fenrich, K. K. y P. K. Rose. "Spinal Interneuron Axons Spontaneously Regenerate after Spinal Cord Injury in the Adult Feline". Journal of Neuroscience 29, n.º 39 (30 de septiembre de 2009): 12145–58. http://dx.doi.org/10.1523/jneurosci.0897-09.2009.

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47

Lurie, Diana I. y Michael E. Selzer. "Preferential regeneration of spinal axons through the scar in hemisected lamprey spinal cord". Journal of Comparative Neurology 313, n.º 4 (22 de noviembre de 1991): 669–79. http://dx.doi.org/10.1002/cne.903130410.

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48

Bregman, Barbara S. "Spinal cord transplants permit the growth of serotonergic axons across the site of neonatal spinal cord transection". Developmental Brain Research 34, n.º 2 (agosto de 1987): 265–79. http://dx.doi.org/10.1016/0165-3806(87)90214-8.

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49

Hao, Hailing y David I. Shreiber. "Axon Kinematics Change During Growth and Development". Journal of Biomechanical Engineering 129, n.º 4 (14 de febrero de 2007): 511–22. http://dx.doi.org/10.1115/1.2746372.

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The microkinematic response of axons to mechanical stretch was examined in the developing chick embryo spinal cord during a period of rapid growth and myelination. Spinal cords were isolated at different days of embryonic (E) development post-fertilization (E12, E14, E16, and E18) and stretched 0%, 5%, 10%, 15%, and 20%, respectively. During this period, the spinal cord grew ∼55% in length, and white matter tracts were myelinated significantly. The spinal cords were fixed with paraformaldehyde at the stretched length, sectioned, stained immunohistochemically for neurofilament proteins, and imaged with epifluorescence microscopy. Axons in unstretched spinal cords were undulated, or tortuous, to varying degrees, and appeared to straighten with stretch. The degree of tortuosity (ratio of the segment’s pathlength to its end-to-end length) was quantified in each spinal cord by tracing several hundred randomly selected axons. The change in tortuosity distributions with stretch indicated that axons switched from non-affine, uncoupled behavior at low stretch levels to affine, coupled behavior at high stretch levels, which was consistent with previous reports of axon behavior in the adult guinea pig optic nerve (Bain, Shreiber, and Meaney, J. Biomech. Eng., 125(6), pp. 798–804). A mathematical model previously proposed by Bain et al. was applied to quantify the transition in kinematic behavior. The results indicated that significant percentages of axons demonstrated purely non-affine behavior at each stage, but that this percentage decreased from 64% at E12 to 30% at E18. The decrease correlated negatively to increases in both length and myelination with development, but the change in axon kinematics could not be explained by stretch applied during physical growth of the spinal cord. The relationship between tissue-level and axonal-level deformation changes with development, which can have important implications in the response to physiological forces experienced during growth and trauma.

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50

Barami, Kaveh y Fernando G. Diaz. "Cellular Transplantation and Spinal Cord Injury". Neurosurgery 47, n.º 3 (1 de septiembre de 2000): 691–700. http://dx.doi.org/10.1097/00006123-200009000-00033.

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ABSTRACT SPINAL CORD INJURY is often characterized by immediate and irreversible loss of sensory and motor functions below the level of injury. Cellular transplantation in various experimental models of spinal cord injury has been used as a strategy for reducing deficits and improving functional recovery. The general strategy has been aimed at promoting regeneration of intrinsic injured axons with the development of alternative pathways that facilitate a partial functional connection. Other objectives of cellular transplantation studies have included replacement of lost cellular elements, alleviation of chronic pain, and modulation of the inflammatory response after injury. This review focuses on the cell types that have been used in spinal cord transplantation studies in the context of evolving biological perspectives, technological advances, and new therapeutic strategies and serves as a point of reference for future studies.

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