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Embryonic Spinal Cord (embryonic + spinal_cord)
Selected AbstractsDifferential 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] Glutamate drives the touch response through a rostral loop in the spinal cord of zebrafish embryosDEVELOPMENTAL NEUROBIOLOGY, Issue 12 2009Thomas Pietri Abstract Characterizing connectivity in the spinal cord of zebrafish embryos is not only prerequisite to understanding the development of locomotion, but is also necessary for maximizing the potential of genetic studies of circuit formation in this model system. During their first day of development, zebrafish embryos show two simple motor behaviors. First, they coil their trunks spontaneously, and a few hours later they start responding to touch with contralateral coils. These behaviors are contemporaneous until spontaneous coils become infrequent by 30 h. Glutamatergic neurons are distributed throughout the embryonic spinal cord, but their contribution to these early motor behaviors in immature zebrafish is still unclear. We demonstrate that the kinetics of spontaneous coiling and touch-evoked responses show distinct developmental time courses and that the touch response is dependent on AMPA-type glutamate receptor activation. Transection experiments suggest that the circuits required for touch-evoked responses are confined to the spinal cord and that only the most rostral part of the spinal cord is sufficient for triggering the full response. This rostral sensory connection is presumably established via CoPA interneurons, as they project to the rostral spinal cord. Electrophysiological analysis demonstrates that these neurons receive short latency AMPA-type glutamatergic inputs in response to ipsilateral tactile stimuli. We conclude that touch responses in early embryonic zebrafish arise only after glutamatergic synapses connect sensory neurons and interneurons to the contralateral motor network via a rostral loop. This helps define an elementary circuit that is modified by the addition of sensory inputs, resulting in behavioral transformation. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009 [source] L1, ,1 integrin, and cadherins mediate axonal regeneration in the embryonic spinal cordDEVELOPMENTAL NEUROBIOLOGY, Issue 14 2006Murray Blackmore Abstract Embryonic birds and mammals are capable of axon regeneration after spinal cord injury, but this ability is lost during a discrete developmental transition. We recently showed that changes within maturing neurons, as opposed to changes solely in the spinal cord environment, significantly restrict axon regeneration during development. The developmental changes within neurons that limit axon regeneration remain unclear. One gap in knowledge is the identity of the adhesive receptors that embryonic neurons use to extend axons in the spinal cord. Here we test the roles of L1/NgCAM, ,1 integrin, and cadherins, using a coculture system in which embryonic chick brainstem neurons regenerate axons into an explant of embryonic spinal cord. By in vivo and in vitro methods, we found that brainstem neurons reduce axonal expression of L1 as they mature. Disrupting either L1 or ,1 integrin function individually in our coculture system partially inhibited growth of brainstem axons in spinal cords, while disrupting cadherin function alone had no effect. However, when all three adhesive receptors were blocked simultaneously, axon growth in the spinal cord was reduced by 90%. Using immunohistochemistry and in situ hybridization we show that during the period when neurons lose their regenerative capacity they reduce expression of mRNA for N-cadherin, and reduce axonal L1/NgCAM protein through a post-transcriptional mechanism. These data show that embryonic neurons use L1/NgCAM, ,1 integrin, and cadherin receptors for axon regeneration in the embryonic spinal cord, and raise the possibility that a reduced expression of these essential receptors may contribute to the low-regenerative capacity of older neurons. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source] Proteasomal inhibition by misfolded mutant superoxide dismutase 1 induces selective motor neuron death in familial amyotrophic lateral sclerosisJOURNAL OF NEUROCHEMISTRY, Issue 5 2002Makoto Urushitani Abstract Accumulating evidence indicates that abnormal conformation of mutant superoxide dismutase 1 (SOD1) is an essential feature underlying the pathogenesis of mutant SOD1-linked familial amyotrophic lateral sclerosis (ALS). Here we investigated the role of ubiquitin-proteasome pathway in the mutant SOD1-related cell death and the effect of oxidative stress on the misfolding of mutant SOD1. Transient overexpression of ubiquitin with human SOD1 (wild-type, ala4val, gly85arg, gly93ala) in Neuro2A cells decreased the amount of mutant SOD1, but not of wild-type, while only mutants were co-immunoprecipitated with poly-ubiquitin. Proteasome inhibition by lactacystin augmented accumulation of mutant SOD1 in the non-ionic detergent-insoluble fraction. The spinal cord lysates from mutant SOD1 transgenic mice showed multiple carbonylated proteins, including mutant SOD1 with SDS-resistant dimer formation. Furthermore, the treatment of hSOD1-expressing cells with hydrogen peroxide promoted the oligomerization, and detergent-insolubility of mutant SOD1 alone, and the oxidized mutant SOD1 proteins were more heavily poly-ubiquitinated. In Neuro2A cells stably expressing human SOD1 protein, the proteasome function measured by chymotrypsin-like activity, was decreased over time without a quantitative alteration of the 20S proteasomal component. Finally, primary motor neurons from the mouse embryonic spinal cord were more vulnerable to lactacystin than non-motor neurons. These results indicate that the sustained expression of mutant SOD1 leads to proteasomal inhibition and motor neuronal death, which in part explains the pathogenesis of mutant SOD1-linked ALS. [source] Gene Expression of Spag6 in Chick Central Nervous SystemANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2010T. Hamada With 5 figures Summary Using a differential display method, we identified sperm-associated antigen 6 (Spag6) as a gene with a dynamic expression profile within the chick embryonic spinal cord. The expression of Spag6 gradually decreased along with spinal cord development. Spag6 expression was detected adjacent to the ventricular zone of the spinal cord at embryonic day (E) 4. At E6, Spag6 was apparent in the ventral ventricular zone adjacent to floor plate and the surrounding region close to the ventricular zone, with additional weak expression at the adjacent region to the ventral horn. At E10, the Spag6 mRNA can be detected slightly in the ventral ventricular zone and surrounding region of dorsal ventricular zone. In the E6 hindbrain, Spag6 was detected in the roof, the ventricular zone adjacent to floor plate and the surrounding regions of the ventricular zones. In the E6 caudal diencephalon, Spag6 expression was detected adjacent to the ventricular zone. As Spag6 was expressed in areas containing ependymal progenitor cells and in the borders of undifferentiated regions, Spag6 may be involved in the development of ependymal cells and in the differentiation process of neuronal cells in chick neural organs. [source] | ||||||||||