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vinblastine/atrofija
Veza se sprema u međuspremnik
Page 1 od 78 rezultati
Topical application of colchicine, vinblastine and vincristine prevents strychnine-enhanced transsynaptic degeneration in the medullary dorsal horn following transection of the inferior alveolar nerve in adult rats.
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The effect of topical application of axonal transport blockers to the transected peripheral nerve was assessed by quantitating the strychnine-enhanced transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats. Systemic administration of strychnine (1 mg/kg/day)
A fine structural study of the formation of temporary swellings (Herring bodies) and reversible degeneration of neurosecretory axons following microiontophoretic ejection of vinblastine into the hypothalamo-neurohypophysial tract of the frog (Rana pipiens).
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The microiontophoretic ejection of vinblastine into the median eminence effectively blocked axonal transport in the hypothalamoneurohypophysial system of the frog. Proximal to the ejection site, large axon swellings (Herring bodies) were found that contained mainly abundant neurosecretory granulated
Effects of colchicine, vinblastine and vincristine on degeneration transmitter release after sympathetic denervation studied in the conscious rat.
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Degeneration contraction after local vinblastine treatment of superior cervical ganglia in the rat.
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Perineural microtubule inhibitors induce degenerative atrophy of central nociceptive terminals in the Rolando substance.
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Short-term perineural application of a microtubule inhibitor around a peripheral nerve induces degenerative atrophy of primary central nociceptive terminals in the Rolando substance. Consequences of the local microtubule inhibitor treatment are identical, both at light- and electron microscopic
Toxicology of vindesine (desacetyl vinblastine amide) in mice, rats, and dogs.
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Comparative acute intravenous toxicity studies of vinblastine sulfate (VLB), vincristine sulfate (VCR), and vindesine in mice and rats indicated that vindesine was more toxic than VLB and less toxic than VCR. Rats were able to tolerate larger repeated doses of vindesine than dogs. Rats given
Selective noradrenergic denervation of the heart following intravenous injections of vinblastine or vincristine.
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1. The progressive effects of a single injection (3mg/kg i.v.) of either vinblastine or vincristine on the innervation of the rat atria have been examined. 2. Functional studies were performed by stimulating electrically the noradrenergic or cholinergic nerve fibres within isolated left atria from
Calpain-mediated cleavage of collapsin response mediator protein(CRMP)-2 during neurite degeneration in mice.
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Axon or dendrite degeneration involves activation of the ubiquitin-proteasome system, failure to maintain neuritic ATP levels, microtubule fragmentation and a mitochondrial permeability transition that occur independently of the somal death programs. To gain further insight into the neurite
Animal models of amyotrophic lateral sclerosis and the spinal muscular atrophies.
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The causes of human amyotrophic lateral sclerosis (ALS) and the spinal muscular atrophies (SMA) are, almost without exception, unknown. This ignorance has stimulated the search for animal models to obtain insight into the etiology, pathogenesis and biochemical mechanisms underlying the human
Effect on the rat hypoglossal nucleus of vinblastine and colchicine applied to the intact or transected hypoglossal nerve.
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The possibility that interruption of axonal transport in otherwise intact axons induces retrograde neuronal and nonneuronal reactions was examined. In addition, the proposal that blockade of axonal transport proximal to nerve injury might inhibit or delay the axon reaction was examined. Cuffs
N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) suppresses neuritic degeneration caused by different experimental paradigms including in vitro Wallerian degeneration.
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Accumulating evidence indicates that neurite degeneration occurs via a distinct mechanism from somal death programs. We have previously shown that neuritic ATP level in sympathetic neurons decreases, whereas somal ATP level remains unaltered during degeneration caused by the microtubule-disrupting
Non-apoptotic neurite degeneration in apoptotic neuronal death: pivotal role of mitochondrial function in neurites.
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The length and thinness of neurites render them greatly susceptible to a variety of insults. Accumulating evidence suggests that neurite degeneration is not a passive, but an active and causative, event in some neurodegenerative diseases. Nonetheless, the mechanisms underlying neurite degeneration
Reversible ultrastructural changes of arcuate neurons after vinblastine injection into the median eminence of the rat.
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The ultrastructural effects of vinblastine on the arcuate neurons and median eminence were studied in the rat. The animals were stereotaxically injected with solutions of 1 mM and 5 mM vinblastine into the median eminence and killed 3, 8 and 21 days after injection. Eight days after injection of 1
Light and electron microscopic observations on rat molar periodontal ligament after intraperitoneal injection of vinblastine.
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The effect of intraperitoneal injection of Vinblastine sulfate on rat periodontal ligament was studied. Cells still synthetize collagen after 2 hours of the injection with evidence of loss of extracellular collagen fibers orientation. Tubular lysosome could not be detected after 2 hours with
Meiotic arrest and aneuploidy induced by vinblastine in mouse oocytes.
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Young superovulated female mice were injected i.p. with single doses of vinblastine sulfate just before the onset of the first meiotic division. Secondary oocytes, fixed one by one on a slide, were cytogenetically scored. Evidence of the meiotic arresting activity of vinblastine was produced by the
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