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In JoVE (1)
Other Publications (2)
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Articles by Seanna M. Martin in JoVE
Dois fótons axotomia e lapso de tempo de imagem confocal em embriões de peixe-zebra ao vivo
Georgeann S. O'Brien1, Sandra Rieger1, Seanna M. Martin1, Ann M. Cavanaugh1, Carlos Portera-Cailliau2, Alvaro Sagasti1
1Department of Molecular Cell and Developmental Biology, University of California, Los Angeles, 2Departments of Neurology and Neurobiology, University of California, Los Angeles
Aqui nós descrevemos um método para a montagem de embriões zebrafish de longo prazo de imagem, de dois fótons de imagem e tecidos de danos técnicas e lapso de tempo de imagem confocal.
Other articles by Seanna M. Martin on PubMed
Developmentally Regulated Impediments to Skin Reinnervation by Injured Peripheral Sensory Axon Terminals
Current Biology : CB. Dec, 2009 | Pubmed ID: 19962310
The structural plasticity of neurites in the central nervous system (CNS) diminishes dramatically after initial development, but the peripheral nervous system (PNS) retains substantial plasticity into adulthood. Nevertheless, functional reinnervation by injured peripheral sensory neurons is often incomplete [1-6]. To investigate the developmental control of skin reinnervation, we imaged the regeneration of trigeminal sensory axon terminals in live zebrafish larvae following laser axotomy. When axons were injured during early stages of outgrowth, regenerating and uninjured axons grew into denervated skin and competed with one another for territory. At later stages, after the establishment of peripheral arbor territories, the ability of uninjured neighbors to sprout diminished severely, and although injured axons reinitiated growth, they were repelled by denervated skin. Regenerating axons were repelled specifically by their former territories, suggesting that local inhibitory factors persist in these regions. Antagonizing the function of several members of the Nogo receptor (NgR)/RhoA pathway improved the capacity of injured axons to grow into denervated skin. Thus, as in the CNS, impediments to reinnervation in the PNS arise after initial establishment of axon arbor structure.
Wallerian Degeneration of Zebrafish Trigeminal Axons in the Skin is Required for Regeneration and Developmental Pruning
Development (Cambridge, England). Dec, 2010 | Pubmed ID: 21041367
Fragments of injured axons that detach from their cell body break down by the molecularly regulated process of Wallerian degeneration (WD). Although WD resembles local axon degeneration, a common mechanism for refining neuronal structure, several previously examined instances of developmental pruning were unaffected by WD pathways. We used laser axotomy and time-lapse confocal imaging to characterize and compare peripheral sensory axon WD and developmental pruning in live zebrafish larvae. Detached fragments of single injured axon arbors underwent three stereotyped phases of WD: a lag phase, a fragmentation phase and clearance. The lag phase was developmentally regulated, becoming shorter as embryos aged, while the length of the clearance phase increased with the amount of axon debris. Both cell-specific inhibition of ubiquitylation and overexpression of the Wallerian degeneration slow protein (Wld(S)) lengthened the lag phase dramatically, but neither affected fragmentation. Persistent Wld(S)-expressing axon fragments directly repelled regenerating axon branches of their parent arbor, similar to self-repulsion among sister branches of intact arbors. Expression of Wld(S) also disrupted naturally occurring local axon pruning and axon degeneration in spontaneously dying trigeminal neurons: although pieces of Wld(S)-expressing axons were pruned, and some Wld(S)-expressing cells still died during development, in both cases detached axon fragments failed to degenerate. We propose that spontaneously pruned fragments of peripheral sensory axons must be removed by a WD-like mechanism to permit efficient innervation of the epidermis.