Spinal Cord Explants Use Carbon Nanotube Interfaces To Enhance Neurite Outgrowth and To Fortify Synaptic Inputs

ACS Nano ◽  
2012 ◽  
Vol 6 (3) ◽  
pp. 2041-2055 ◽  
Author(s):  
Alessandra Fabbro ◽  
Ambra Villari ◽  
Jummi Laishram ◽  
Denis Scaini ◽  
Francesca M. Toma ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Carbon Nanotube ◽  
Neurite Outgrowth ◽  
Synaptic Inputs ◽  
Enhance Neurite Outgrowth

Thermally sensitive conductive hydrogel using amphiphilic crosslinker self-assembled carbon nanotube to enhance neurite outgrowth and promote spinal cord regeneration

RSC Advances ◽  
2016 ◽  
Vol 6 (31) ◽  
pp. 26341-26351 ◽  
Author(s):  
Lili Sang ◽  
Yuqing Liu ◽  
Wenxi Hua ◽  
Kaige Xu ◽  
Guobao Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Carbon Nanotube ◽  
Neurite Outgrowth ◽  
Potential Role ◽  
Spinal Cord Regeneration ◽  
Conductive Hydrogel ◽  
Self Assembled ◽  
Enhance Neurite Outgrowth

We studied a SWNT–PNIPAAM hydrogel for its potential role in the growth of SH-SY5Y cells and found it can enhance neurite outgrowth when adding electrical stimulation in vitro.

Changes in properties of lamprey reticulospinal neurons following spinal cord injury

2015 ◽  
Author(s):  
◽  
Timothee Pale
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Properties ◽  
Neurite Outgrowth ◽  
Axonal Transport ◽  
Axonal Regeneration ◽  
Retrograde Axonal Transport ◽  
Slight Reduction ◽  
Synaptic Inputs ◽  
Cord Injury

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] The lamprey is one of the most ancient vertebrates, sharing many of basic characteristics of the brain and spinal cord with higher, more evolved vertebrates such as mammals. However, unlike humans and other higher vertebrates, lampreys display robust axonal regeneration in the central nervous system following spinal cord injury (SCI). For instance, axons of reticulospinal (RS) neurons in the brain can regenerate and reconnect with spinal targets leading to recovery of locomotor behavior within a few weeks following SCI. During axonal regeneration, at [about]2-3 weeks following SCI, injured RS neurons display dramatic changes in their electrical properties (i.e. "injury phenotype", absence of 2/3 afterpotentials) compared to uninjured neurons. These changes may be due to axonal injury itself, interruption of retrograde axonal transport, and/or changes in synaptic inputs. The present work will focus on several aspects of lamprey RS neurons following SCI. (1) Can activation of second messenger signaling pathways stimulate neurite outgrowth of lamprey RS neurons without altering their electrical properties? (2) Does axotomy affect Ca2+ and SK channels and their underlying conductances? (3) Are the changes in biophysical properties of RS neurons following SCI due, in part, to disruption of retrograde axonal transport? (4) Does SCI lead to changes in morphology and synaptic inputs of injured lamprey RS neurons? For lamprey RS neurons in culture, activation of cAMP pathways stimulated neurite outgrowth. In brainspinal cord preparations, forskolin resulted in action potential broadening, at least for uninjured RS neurons, which would very likely increase calcium influx. In contrast, for lamprey RS neurons, dbcAMP stimulated neurite outgrowth without altering their electrical properties. These results suggest that activation of cAMP signaling may be an effective approach for stimulating axonal regeneration of RS neurons following spinal cord injury. Our results suggest that there may be little differences in Ca2+ currents and SK currents between injured and uninjured large RS neurons. Perhaps the slight reduction in the total Ca2+ influx combined with a slight reduction of SK current (fewer activated by Ca2+) is responsible for the abolishment of the sAHP in lamprey RS neurons [about]2-3 weeks following injury. In uninjured large RS neurons that were not physically damaged by the application of the microtubuledisrupting agent vinblastine, blocking retrograde axonal transport caused some neurons to fire erratically and display the "injury phenotype", which is typical for axotomized neurons following SCI. These results suggest that retrograde axonal transport may play an important role in the maintenance of normal electrical properties in uninjured lamprey large RS neurons. Additionally, these results suggest that following SCI, interruption of retrograde axonal transport perhaps contributes to the changes in electrical properties (i.e "injury phenotype") in injured lamprey RS neurons. Injured large RS neurons did not display significant differences in the amplitudes of their synaptic responses from stimulation of the oral hood compared to uninjured neurons whether they were stimulated contralaterally or ipsilaterally, and synaptic responses of injured and uninjured RS neurons from stimulations on either the right or the left side of the oral hood were not significantly different. Taken together, these results suggest that injury does not substantially alter the synaptic inputs of injured large RS neurons. Following rostral SCI in lampreys, large injured RS neurons did not display significant changes in their basic morphology of lamprey large RS neurons. For example, the major and minor diameters of injured large RS neurons were not significantly different than those of uninjured neurons. In addition, compared to uninjured neurons, injured neurons did not have different number of primary and secondary dendrites. These results suggest that SCI does not substantially alter the basic morphology of large lamprey RS neurons. The present work provided a better understanding of the mechanisms underlying the biophysical changes of injured lamprey RS neurons during axonal regeneration. These findings could help in the development of novel therapeutic strategies to enhance axonal regeneration, following spinal cord injury in higher vertebrates, including perhaps humans.

Acidic and basic fibroblast growth factors enhance neurite outgrowth in cultured rat spinal cord neurons

1995 ◽  
Vol 17 (1) ◽  
pp. 70-72 ◽  
Author(s):  
Yasuo Iwasaki ◽  
Toshiya Shiojima ◽  
Ken Ikeda ◽  
Nozomu Tagaya ◽  
Tomoko Kobayashi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Growth Factors ◽  
Neurite Outgrowth ◽  
Fibroblast Growth Factors ◽  
Fibroblast Growth ◽  
Rat Spinal Cord ◽  
Spinal Cord Neurons ◽  
Enhance Neurite Outgrowth

scholarly journals EphA4 Obstructs Spinal Cord Neuron Regeneration by Promoting Excessive Activation of Astrocytes

2021 ◽  
Author(s):  
Xiaogang Chen ◽  
Lin Zhang ◽  
Fu Hua ◽  
Yu Zhuang ◽  
Huan Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Growth Factor ◽  
Neurite Outgrowth ◽  
Neurotrophic Factors ◽  
Cellular Localization ◽  
Axon Regeneration ◽  
Chondroitin Sulphate ◽  
Cortical Cell ◽  
Inflammatory Factors ◽  
Cord Injury

AbstractStudies have found that molecular targets that regulate tissue development are also involved in regulating tissue regeneration. Erythropoietin-producing hepatocyte A4 (EphA4) not only plays a guiding role in neurite outgrowth during the development of the central nervous system (CNS) but also induces injured axon retraction and inhibits axon regeneration after spinal cord injury (SCI). EphA4 targets several ephrin ligands (including ephrin-A and ephrin-B) and is involved in cortical cell migration, axon guidance, synapse formation and astrocyte function. However, how EphA4 affects axon regeneration after SCI remains unclear. This study focuses on the effect and mechanism of EphA4-regulated astrocyte function in neuronal regeneration after SCI. Our research found that EphA4 expression increased significantly after SCI and peaked at 3 days post-injury; accordingly, we identified the cellular localization of EphA4 and ephrin-B ligands in neurons and astrocytes after SCI. EphA4 was mainly expressed on the surface of neurons, ephrin-B1 and ephrin-B3 were mainly localized on astrocytes, and ephrin-B2 was distributed on both neurons and astrocytes. To further elucidate the effect of EphA4 on astrocyte function after SCI, we detected the related cytokines secreted by astrocytes in vivo. We found that the levels of neurotrophic factors including nerve growth factor (NGF) and basic fibroblast growth factor (bFGF) increased significantly after SCI (NGF peaked at 3 days and bFGF peaked at 7 days); the expression of laminin and fibronectin increased gradually after SCI; the expression of inflammatory factors [interleukin (IL)-1β and IL-6] increased significantly from 4 h to 7 days after SCI; and the levels of glial fibrillary acidic protein (GFAP), a marker of astrocyte activation, and chondroitin sulphate proteoglycan (CSPG), the main component of glial scars, both peaked at 7 days after SCI. Using a damaged astrocyte model in vitro, we similarly found that the levels of related cytokines increased after injury. Consequently, we observed the effect of damaged astrocytes on neurite outgrowth and regeneration, and the results showed that damaged astrocytes hindered neurite outgrowth and regeneration; however, the inhibitory effect of injured astrocytes on neurite regeneration was reduced following ephrin-B receptor knockdown or inflammatory inhibition at 24 h after astrocyte injury. Our results showed that EphA4 regulates the secretion of neurotrophic factors, adhesion molecules, inflammatory factors and glial scar formation by binding with the ligand ephrin-B located on the surface of astrocytes. EphA4 affects neurite outgrowth and regeneration after SCI by regulating astrocyte function.

Muscle-conditioned media and cAMP promote survival and neurite outgrowth of adult spinal cord motor neurons

2009 ◽  
Vol 220 (2) ◽  
pp. 303-315 ◽  
Author(s):  
Jose V. Montoya G. ◽  
Jhon Jairo Sutachan ◽  
Wai Si Chan ◽  
Alexandra Sideris ◽  
Thomas J.J. Blanck ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neurite Outgrowth ◽  
Motor Neurons ◽  
Conditioned Media ◽  
Adult Spinal Cord
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