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Cord Neurons (cord + neuron)
Kinds of Cord Neurons Selected AbstractsCanine Spinal Cord Neuron and Axon Myelin Sheath MorphometryANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2006A. C. De Francischini Carvalho Summary This inedited morphometric study has been developed from healthy canine spinal cord neuron cytoplasm and nucleus, and white matter axonal myelin sheath, from cervical, thoracic and lumbar regions. For the morphometric study, the parameters were area, perimeter, maximum and minimum diameters and roundness for neurons and myelin thickness for axon. For each parameter, 300 neurons were analysed. The results revealed that lumbar neurons had the highest mean values for the analysed parameters, indicating the presence of large neurons in this region, with large axons as a result of myelin thickness, which is proportional to axon calibre. We conclude that these morphometric results can contribute for the establishment of normal patterns, for canine spinal cord cervical, thoracic and lumbar segments. [source] Differential expression and localization of neuronal intermediate filament proteins within newly developing neurites in dissociated cultures of Xenopus laevis embryonic spinal cordCYTOSKELETON, Issue 1 2001Jayanthi Undamatla Abstract The molecular subunit composition of neurofilaments (NFs) progressively changes during axon development. In developing Xenopus laevis spinal cord, peripherin emerges at the earliest stages of neurite outgrowth. NF-M and XNIF (an ,-internexin-like protein) appear later, as axons continue to elongate, and NF-L is expressed after axons contact muscle. Because NFs are the most abundant component of the vertebrate axonal cytoskeleton, we must understand why these changes occur before we can fully comprehend how the cytoskeleton regulates axon growth and morphology. Knowing where these proteins are localized within developing neurites and how their expression changes with cell contact is essential for this understanding. Thus, we examined by immunofluorescence the expression and localization of these NF subunits within dissociated cultures of newly differentiating spinal cord neurons. In young neurites, peripherin was most abundant in distal neuritic segments, especially near branch points and extending into the central domain of the growth cone. In contrast, XNIF and NF-M were usually either absent from very young neurites or exhibited a proximal to distal gradient of decreasing intensity. In older neurites, XNIF and NF-M expression increased, whereas that of peripherin declined. All three of these proteins became more evenly distributed along the neurites, with some branches staining more intensely than others. At 24 h, NF-L appeared, and in 48-h cultures, its expression, along with that of NF-M, was greater in neurites contacting muscle cells, arguing that the upregulation of these two subunits is dependent on contact with target cells. Moreover, this contact had no effect on XNIF or peripherin expression. Our findings are consistent with a model in which peripherin plays an important structural role in growth cones, XNIF and NF-M help consolidate the intermediate filament cytoskeleton beginning in the proximal neurite, and increased levels of NF-L and NF-M help further solidify the cytoskeleton of axons that successfully reach their targets. Cell Motil. Cytoskeleton 49:16,32, 2001. © 2001 Wiley-Liss, Inc. [source] Two Na,K-ATPase ,2 subunit isoforms are differentially expressed within the central nervous system and sensory organs during zebrafish embryogenesisDEVELOPMENTAL DYNAMICS, Issue 2 2002Johannes R. Rajarao Abstract We have identified cDNAs encoding a second zebrafish ortholog of the human Na,K-ATPase ,2 subunit. The ,2b cDNA encodes a 292 amino acid-long polypeptide with 74% identity to the previously characterized zebrafish ,2a subunit. By using a zebrafish meiotic mapping panel, we determined that the ,2b gene (atp1b2b) was tightly linked to markers on linkage group 5, whereas the ,2a gene was located on linkage group 23. In situ hybridization analysis shows that in developing zebrafish embryos, atp1b2a and atp1b2b are predominantly expressed in the nervous system. ,2a transcripts were abundantly expressed throughout brain as well as spinal cord neurons and lateral line ganglia. In contrast, ,2b mRNA expression was primarily detected in sensory organs, including retina, otic vesicles, and lateral line neuromast cells. These results suggest that the ,2a and ,2b genes play distinct roles in developing brain and sensory organs, and raise the possibility that the functions encoded by the single mammalian ,2 gene may be partitioned between the two zebrafish ,2 orthologs. © 2002 Wiley-Liss, Inc. [source] Astroglia-mediated effects of uric acid to protect spinal cord neurons from glutamate toxicityGLIA, Issue 5 2007Yangzhou Du Abstract Uric acid (UA) has been demonstrated to reduce damage to neurons elicited by oxidative stress. However, our studies utilizing cultures derived from embryonic rat spinal cord indicate that an astroglia-mediated mechanism is involved in the effects of UA to protect neurons from glutamate toxicity. The damage elicted by glutamate to neurons in a mixed culture of spinal cord cells can be reversed by UA. Furthermore, addition of UA after the termination of glutamate exposure suggests that UA plays an active role in mediating neuroprotection rather than purely binding peroxynitrite, as previously thought. Importantly, in pure neuron cultures from the same tissue, UA does not protect against glutamate toxicity. Addition of astroglia to the pure neuron cultures restores the ability of UA to protect the neurons from glutamate-induced toxicity. Our results also suggest that glia provide EAAT-1 and EAAT-2 glutamate transporters to protect neurons from glutamate, that functional EAATs may be necessary to mediate the effects of UA, and that treatment with UA results in upregulation of EAAT-1 protein. Taken together, our data strongly suggest that astroglia in mixed cultures are essential for mediating the effects of UA, revealing a novel mechanism by which UA, a naturally produced substance in the body, may act to protect neurons from damage during insults such as spinal cord injury. © 2007 Wiley-Liss, Inc. [source] ERK 1/2 signaling pathway is involved in nicotine-mediated neuroprotection in spinal cord neuronsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2007Michal Toborek Abstract Evidence indicates that agonists of neuronal nicotinic receptors (nAChRs), including nicotine, can induce neuroprotective and anti-apoptotic effects in the CNS. To study these mechanisms, the present study focused on nicotine-mediated modulation of the extracellular regulated kinase 1 and 2 (ERK1/2) pathway in cultured spinal cord neurons. Exposure to nicotine (0.1,10 µM) for as short as 1 min markedly upregulated levels of phosphorylated ERK1/2 (pERK1/2) and increased total ERK1/2 activity. Inhibition studies with mecamylamine and ,-bungarotoxin revealed that these effects were mediated by the ,7 nicotinic receptor. In addition, pre-exposure to U0126, a specific inhibitor of the ERK1/2 signaling, prevented nicotine-mediated anti-apoptotic effects. To indicate if treatment with nicotine also can activate ERK1/2 in vivo, a moderate spinal cord injury (SCI) was induced in rats using a weight-drop device and nicotine was injected 2 h post-trauma. Consistent with in vitro data, nicotine increased levels of pERK1/2 in this animal model of spinal cord trauma. Results of the present study indicate that the ERK1/2 pathway is involved in anti-apoptotic effects of nicotine in spinal cord neurons and may be involved in therapeutic effects of nicotine in spinal cord trauma. J. Cell. Biochem. 100: 279,292, 2007. © 2006 Wiley-Liss, Inc. [source] Nicotine up-regulates expression of neurotrophic factors and attenuates apoptosis of spinal cord neuronsJOURNAL OF NEUROCHEMISTRY, Issue 2003R. Garrido Nicotine may induce neuroprotection in spinal cord injury; however, the mechanisms of these effects are not fully understood. The present study focused on the effects of nicotine on expression of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (FGF-2) in a model of spinal cord injury. In this model, cultured spinal cord neurons are exposed to 10 mm arachidonic acid (AA). Exposure to AA diminished expression of BDNF and FGF-2; however, pretreatment with nicotine protected against these effects. Mecamylamine and ,-bungarotoxin inhibited nicotine-mediated up-regulation of BDNF and FGF-2. Moreover, nicotine, BDNF and FGF-2 protected against AA-induced apoptosis of spinal cord neurons. These results suggest that AA can induce apoptosis of spinal cord neurons by depletion of neurotrophic factors and that nicotine can protect against these effects through the alpha7 receptor-mediated pathway. Acknowledgements:, Supported by grants from Philip Morris Research Program and KSCHIRT. [source] Macrophage migration inhibitor factor (MIF) can induce oxidative injury and apoptotic cell death of spinal cord neuronsJOURNAL OF NEUROCHEMISTRY, Issue 2003M. Toborek MIF is a cytokine produced by a variety of cells and tissues including the CNS. It can exert a variety of biological functions, such as induction of inflammatory responses and counterregulation of glucocorticoid effects. However, the role of MIF in the pathogenesis of spinal cord trauma is not fully understood. Therefore, the aim of the present study was to evaluate the cellular effects of MIF in cultured spinal cord neurons. A 3-h exposure to MIF significantly enhanced intracellular calcium levels; an effect which was prevented by TMB-8, an antagonist of the IP3 receptor. In addition, MIF treatment increased oxidative stress, decreased viability of spinal cord neurons, increased LDH release and stimulated apoptosis. These results suggest that MIF may play an important role in secondary spinal cord injury. Acknowledgements:, Supported by grants from KSCHIRT and Philip Morris External Research Program. [source] Therapeutic benefits of intrathecal protein therapy in a mouse model of amyotrophic lateral sclerosisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 13 2008Yasuyuki Ohta Abstract When fused with the protein transduction domain (PTD) derived from the human immunodeficiency virus TAT protein, proteins can cross the blood,brain barrier and cell membrane and transfer into several tissues, including the brain, making protein therapy feasible for various neurological disorders. We have constructed a powerful antiapoptotic modified Bcl-XL protein (originally constructed from Bcl-XL) fused with PTD derived from TAT (TAT-modified Bcl-XL), and, to examine its clinical effectiveness in a mouse model of familial amyotrophic lateral sclerosis (ALS), transgenic mice expressing human Cu/Zn superoxide dismutase (SOD1) bearing a G93A mutation were treated by intrathecal infusion of TAT-modified Bcl-XL. We demonstrate that intrathecally infused TAT-fused protein was effectively transferred into spinal cord neurons, including motor neurons, and that intrathecal infusion of TAT-modified Bcl-XL delayed disease onset, prolonged survival, and improved motor performance. Histological studies show an attenuation of motor neuron loss and a decrease in the number of cleaved caspase 9-, cleaved caspase 3-, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in the lumbar cords of TAT-modified Bcl-XL -treated G93A mice. Our results indicate that intrathecal protein therapy using a TAT-fused protein is an effective clinical tool for the treatment of ALS. © 2008 Wiley-Liss, Inc. [source] Expressions of nitrotyrosine and TUNEL immunoreactivities in cultured rat spinal cord neurons after exposure to glutamate, nitric oxide, or peroxynitriteJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2001Y. Manabe Abstract Although excitotoxic and oxidative stress play important roles in spinal neuron death, the exact mechanism is not fully understood. We examined cell damage of primary culture of 11-day-old rat spinal cord by addition of glutamate, nitric oxide (NO) or peroxynitrite (PN) with detection of nitrotyrosine (NT) or terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL). With addition of glutamate, NOC18 (a slow NO releaser) or PN, immunoreactivity for NT became stronger in the cytoplasm of large motor neurons in the ventral horn at 6 to 48 hr and positive in the axons of the ventral horn at 24 to 48 hr. TUNEL positive nuclei were found in spinal large motor neurons from 24 hr, and the positive cell number greatly increased at 48 hr in contrast to the vehicle. Pretreatment of cultures with ,-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor antagonist, NO-suppressing agent, and antioxidant protected the immunoreactivity for NT or TUNEL. The present results suggest that both excitotoxic and oxidative stress play an important role in the upregulation of NT nitration and the apoptotic pathway in cultured rat spinal neurons. J. Neurosci. Res. 65:371,377, 2001. © 2001 Wiley-Liss, Inc. [source] | ||||||||||