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Rat Organ (rat + organ)
Selected AbstractsDifferential expression of PKC beta II in the rat organ of CortiEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2007S. Ladrech Abstract To investigate a possible involvement of protein kinase C (PKC) in cochlear efferent neurotransmission, we studied the expression of the calcium-dependent PKC beta II isoform in the rat organ of Corti at different postnatal ages using immunofluorescence and immunoelectron microscopy. We found evidence of PKC beta II as early as postnatal day (PND) 5 in efferent axons running in the inner spiral bundle and in Hensen cells. At PND 8, we also found PKC beta II in efferents targeting outer hair cells (OHCs), and a slight detection at the synaptic pole in the first row of the basal and middle cochlear turns. At PND 12, PKC beta II expression declined in the efferent fibres contacting OHCs, whereas expression was concentrated at the postsynaptic membrane, from the basal and middle turns. The adult-like pattern of PKC beta II distribution was observed at PND 20. Throughout the cochlea, we found PKC beta II expression in the Hensen cells, non-sensory cells involved in potassium re-cycling, and lateral efferent terminals of the inner spiral bundle. In addition, we observed expression in OHCs at the postsynaptic membrane facing the endings of the medial efferent system, with the exception of some OHCs located in the most apical region of the cochlea. These data therefore suggest an involvement of PKC beta II in both cochlear efferent neurotransmission and ion homeostasis. Among other functions, PKC beta II could play a role in the efferent control of OHC activity. [source] Macrophage contribution to the response of the rat organ of Corti to amikacinJOURNAL OF NEUROSCIENCE RESEARCH, Issue 9 2007Sabine Ladrech Abstract Transdifferentiation of nonsensory supporting cells into sensory hair cells occurs naturally in the damaged avian inner ear. Such transdifferentiation was achieved experimentally in the cochlea of deaf guinea pigs through Atoh 1 gene transfection. Supporting cells may therefore serve as targets for transdifferentiation therapy. Supporting cells rapidly degenerate after hair cell disappearance, however, limiting the therapeutic window for gene transfer. We studied the time course of ultrastructural and phenotypical changes occurring in Deiters cells (hair cell supporting cells) after ototoxic treatment in the rat. The presence of macrophages in the cochlea was also investigated, to study any deleterious effects they may have on pathologic tissues. One week after treatment most hair cells had disappeared. Deiters cells no longer expressed the glial marker vimentin but instead displayed typical hair cell markers, the calcium binding proteins calbindin and parvalbumin. This suggests that a process of transdifferentiation of Deiters cells into hair cells was activated. By 3 weeks post-treatment, however, the Deiters cells began to degenerate and by 10 weeks post-treatment the organ of Corti was degraded fully. Interestingly, a marked increase in macrophage density was seen after the end of amikacin treatment to 10 weeks post-treatment. This suggests chronic inflammation is involved in epithelium degeneration. Consequently, early treatments with anti-inflammatory factors might promote supporting cell survival, thus improving the efficacy of more specific strategies aimed to regenerate hair cells from nonsensory cells. © 2007 Wiley-Liss, Inc. [source] Microsurgical tracheotomy: A pediatric model in growing ratsMICROSURGERY, Issue 5 2003Mônica Cecília Bochetti Manna M.D. Previous studies described controversial opinions about pediatric tracheotomy concerning type of tracheal incision and long-term results, which remain as important research subjects. Experimental studies on rat tracheas are scarce, probably because of technical difficulties related to the structures' small dimensions. As many rat organ and system operative procedures were studied successfully by using microsurgical techniques, we decided to develop a pediatric tracheotomy model in growing rats which would permit long-term studies. Forty-four Wistar EPM-1 growing rats weighing 86 g and aged 35 days were divided into three groups: submitted to longitudinal, transverse, and segment excision of the trachea. Under sterile technique and intramuscular anesthesia (ketamine/xylazine), the trachea was exposed and incised, according to group, and a hand-made endotracheal cannula was inserted into the organ. This cannula was assembled using a segment of 1.5-cm-long 3 French silicone catheter passed through hexagonal-shaped silicone screen. The tracheal cannula was removed after 7 days, when we evaluated body weight, secretions, and dehiscence. In conclusion, this microsurgical tracheotomy model in growing rats is feasible, allowing studies on long-term repercussions of pediatric tracheotomy. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:530,534 2003 [source] Effects of nickel poisoning on expression pattern of the 72/73 and 94 kDa stress proteins in rat organs and in the COS-7, HepG2, and A549 cell linesJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 1 2005N. Hfaiedh Abstract The present study deals with the effects of Ni on the expression level of three stress proteins, namely, the cytosolic HSP72 and HSP73, and the reticulum-associated GRP94. Experiments were carried out on "Wistar" female rats daily injected with 4 mg NiCl2 per kg body weight for 1, 3, 5, and 10 days. Another set of experiments were carried out using cell lines, derived from the monkey kidney (COS-7), and from human tumors of the lung (A549) and liver (HepG2). Cells were cultured for 4 days in the permanent presence of 100, 200, or 400 µM NiCl2. In control rats, stress proteins pattern was found to be tissue specific: two protein bands of 96 and 94 kDa were immunodetected with the anti-GRP94 antibody in kidney and liver extracts, whereas only the 96 kDa band was present in ovary extracts. HSP73 was present in kidney, liver, and ovary whereas HSP72 was only found in kidney. In kidney of nickel-treated animals, HSP73 and the 96 kDa proteins were overexpressed whereas HSP72 was strongly down regulated. No such effect was observed in liver or ovary. Similarly, in nickel-treated cell lines, HSP72 was downregulated and GRP94 (96 kDa protein) was overexpressed. HSP73 expression appeared moderately increased in A549 cells but decreased in COS-7 cells. Because long-term caloric restriction was reported to reduce free radical generation in cells, the effect of 1 month food restriction (50%) was tested in rats as a possible way to lower oxidative damages induced by Ni. No significant effect on HSP expression was observed. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:12,18, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20056 [source] | ||||||||||