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colchicine/atrophy
Veza se sprema u međuspremnik
Stranica 1 iz 237 rezultatima
Retinal atrophy induced by intravitreous colchicine.
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Colchicine is known to inhibit axoplasmic transport in ganglion cells. Previous studies have shown considerable, but largely reversible, retinal changes after low dosages of intravitreal colchicine in experimental animals. In the present study, the effects of 1.0 to 100 micrograms of intravitreal
Colchicine-induced degeneration of the micronucleus during conjugation in Tetrahymena.
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One of the most dramatic examples of nuclear morphogenesis occurs during conjugation in Tetrahymena when the micronucleus elongates to a size longer than the cell itself. After contraction to a spherical shape, the nucleus moves directly to chromosome separation in the first meiotic division. Here
[Degeneration of the laminated corpuscles (of Vater--Pacini) following colchicine application to a nerve].
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Laminated pacinian corpuscles from the cat mesentery have been studied morphologically and morphometrically after nerve section and colchicine application to the nerve and the results obtained are represented. Similar interventions in the nerve produce changes in the receptors resembling those of
Nerve degeneration is prevented by a single intraneural apotransferrin injection into colchicine-injured sciatic nerves in the rat.
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In this work, we have immunohistochemically analyzed the effects of single injections of apotransferrin (aTf) on the expression of myelin (myelin basic proteins [MBPs]) and axonal (protein gene product 9.5 [PGP 9.5] and beta(III)-tubulin [beta(III)-tub]) proteins in colchicine-injected and crushed
Elimination of granular cells after intrahippocampal colchicine injection causing disappearance of evoked potentials and deterioration of development of the conditioned avoidance reflex in rats.
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The aim of our work was to study the involvement, in the process of learning, of synapses between the perforant path and granular cells of the hippocampal dentate fascia for formation of a conditioned reflex (CR) of active avoidance elaborated in response to electrostimulation of the perforant path.
[Switching off of granule cells after intrahippocampal injection of colchicine eliciting the disappearance of evoked potentials and a deterioration in the development of a conditioned avoidance reflex in rats].
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The aim of the work was to study the involvement in the process of learning of synapses between the perforant path and granular cells of the hippocampal dentate fascia for formation of conditioned reflex (CR) of active avoidance elaborated in response to electrostimulation of the perforant path. For
Retrograde degeneration and colchicine protection of basal forebrain cholinergic neurons following hippocampal injections of an immunotoxin against the P75 nerve growth factor receptor.
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Intracerebroventricular injection of 192 IgG antibody against the p75LNGFR rat low affinity nerve growth factor receptor conjugated with saporin, a ribosome inactivating protein, has been shown to destroy the p75LNGFR-expressing cholinergic neurons of the basal forebrain. We injected this
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)
ZnT3 Gene Deletion Reduces Colchicine-Induced Dentate Granule Cell Degeneration.
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Our previous study demonstrated that colchicine-induced dentate granule cell death is caused by blocking axonal flow and the accumulation of intracellular zinc. Zinc is concentrated in the synaptic vesicles via zinc transporter 3 (ZnT3), which facilitates zinc transport from the cytosol into the
Intrastriatal injection of colchicine induces striatonigral degeneration in mice.
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Recent studies from environmental toxicology and molecular genetics demonstrate that midbrain dopamine (DA) neurons are particularly vulnerable to microtubule depolymerizing agents, indicating the involvement of microtubule dysfunction in the pathogenesis of Parkinson's disease. Here we show that
Time course of degeneration of short and long postganglionic sympathetic nerve fibres and effect of pentobarbitone and colchicine on degeneration.
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1 The time-course of degeneration of sympathetic nerves was investigated by measurement of the endogenous noradrenaline content of the rat vas deferens, submandibular gland and spleen following sympathectomy.2 Extirpation of the hypogastric plexus, superior cervical ganglion and coeliac plexus under
Atrophy of the striatum and motor disturbance induced by colchicine.
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To determine the functional role of the striatonigral system in the circling behavior of rats and the mode of action of colchicine, we investigated the circling behavior induced by dopamine agonists after microinjection of colchicine into the unilateral striatum. Both apomorphine and methamphetamine
Neuronal degeneration and iNOS expression in experimental brain contusion following treatment with colchicine, dexamethasone, tirilazad mesylate and nimodipine.
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BACKGROUND
The pathophysiological mechanisms of secondary neurological injury after traumatic brain injury are complex. Post-traumatic biochemical reactions include parenchymal inflammation, free radical production, increased intracellular calcium and lipid peroxidation and nitric oxide production.
Colchicine induced intraneuronal free zinc accumulation and dentate granule cell degeneration.
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Colchicine has been discovered to inhibit many inflammatory processes such as gout, familial Mediterranean fever, pericarditis and Behcet disease. Other than these beneficial anti-inflammatory effects, colchicine blocks microtubule-assisted axonal transport, which results in the selective loss of
Effects of colchicine, vinblastine and vincristine on degeneration transmitter release after sympathetic denervation studied in the conscious rat.
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