Effect of colchicine on transport of amine storage granules in sympathetic nerves of rat. Eur
ABSTRACT Local application of colchicine to adrenergic ganglia and axons seems to interrupt the fast proximo-distal transport of amine storage granules. This effect may be due to destruction of neurotubules, which possibly take part in granular transport.
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- "Moreover, to our knowledge, there are no reports about the sensitivity of CTB to colchicine, which is a fundamental experiment for whether a tracer travels by active transport . Colchicine is a compound that disrupts microtubules [48–50], therefore it can be used to assay the integrity of active axonal transport [32,47,51–54]. Microtubules within RGC axons are rapidly disrupted when colchicine is administered by intravitreal injection [55–58]. "
ABSTRACT: A technique was developed for assaying axonal transport in retinal ganglion cells using 2 µl injections of 1% cholera toxin b-subunit conjugated to AlexaFluor488 (CTB). In vivo retinal and post-mortem brain imaging by confocal scanning laser ophthalmoscopy and post-mortem microscopy were performed. The transport of CTB was sensitive to colchicine, which disrupts axonal microtubules. The bulk rates of transport were determined to be approximately 80–90 mm/day (anterograde) and 160 mm/day (retrograde). Results demonstrate that axonal transport of CTB can be monitored in vivo in the rodent anterior visual pathway, is dependent on intact microtubules, and occurs by active transport mechanisms.Biomedical Optics Express 02/2013; 4(2):364-86. DOI:10.1364/BOE.4.000364 · 3.50 Impact Factor
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- "We have also examined the e¡ect of nicergoline on degeneration of cholinergic neurons due to NGF deprivation induced by colchicine administration . Colchicine, a mitotic/microtubule inhibitor that binds to tubulin (Borisy and Taylor, 1967) and blocks axoplasmic transport (Dahlstrom, 1968; Kreutzberg, 1969), has been shown to be toxic for certain neural populations including choline acetyltransferase (ChAT)positive neurons (Ginn and Peterson, 1990; Calza © et al., 1997). This e¡ect involves NGF, whose axonal retrograde transport is inhibited by the tubulin block. "
ABSTRACT: The aging brain is characterized by selective neurochemical changes involving several neural populations. A deficit in the cholinergic system of the basal forebrain is thought to contribute to the development of cognitive symptoms of dementia. Attempts to prevent age-associated cholinergic vulnerability and deterioration therefore represent a crucial point for pharmacotherapy in the elderly. In this paper we provide evidence for the protective effect of nicergoline (Sermion®) on the degeneration of cholinergic neurons induced by nerve growth factor deprivation. Nerve growth factor deprivation was induced by colchicine administration in rats 13 and 18 months old. Colchicine induces a rapid and substantial down-regulation of choline acetyltransferase messenger RNA level in the basal forebrain in untreated adult, middle-aged and old rats. Colchicine failed to cause these effects in old rats treated for 120 days with nicergoline 10 mg/kg/day, orally. Moreover, a concomitant increase of both nerve growth factor and brain-derived neurotrophic factor content was measured in the basal forebrain of old, nicergoline-treated rats. Additionally, the level of messenger RNA for the brain isoform of nitric oxide synthase in neurons of the basal forebrain was also increased in these animals.Based on the present findings, nicergoline proved to be an effective drug for preventing neuronal vulnerability due to experimentally induced nerve growth factor deprivation.Neuroscience 02/2002; 109(3-109):487-497. DOI:10.1016/S0306-4522(01)00470-5 · 3.33 Impact Factor
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- "Of interest in this discussion are findings by Cortés et al. (1990) who demonstrated that colchicine treatment in fact increased ppGAL mRNA levels in the ventral forebrain and in the dorsal raphe region (and in several other brain regions), suggesting that this drug can increase peptide synthesis in these systems. Thus, the demonstration of GAL-LI in these two cell groups after colchicine was not only a result of arrest of axonal transport (Dahlström, 1968; Kreutzberg, 1969) but also due to up-regulation of GAL mRNA levels. In summary, very low GAL production under normal circumstances could explain the lack of detectable levels in several ascending systems. "
ABSTRACT: By using immunofluorescence methodology, extensive galanin (GAL) and GAL message-associated peptide (GMAP)-positive terminal networks were observed in the hippocampal formation. The majority of the GAL/GMAP fibers were dopamine β-hydroxylase- (DBH) positive, that is, they were noradrenergic. This finding was established with GAL/GMAP-DBH double-staining and with 6-hydroxy-dopamine treatment, which totally abolished all fibers in which GAL/GMAP and DBH coexisted. Also, reserpine treatment caused a marked depletion of GAL. No evidence for GAL/GMAP coexistence with 5-hydroxytryptamine was obtained. In the ventral hippocampus, GAL/GMAP-, DBH-negative fibers were seen in the stratum oriens, the anterior stratum radiatum, along the granule cell layer and in the strata oriens and alveus. In the locus coeruleus (LC), around 80% of the GMAP-positive neurons contained neuropeptide tyrosine (NPY), and about 40% of the NPY-positive neurons expressed GMAP. GAL-R1 receptor mRNA was expressed in Barrington's nucleus (close to the LC), but was not detected in the hippocampal formation/dorsal cortical areas. GAL-R2 receptor mRNA was found in the granule cell layer in the dentate gyrus.The present results show that most, but not all, immunohistochemically detectable GAL/GMAP in the hippocampal formation/dorsal cortex is present in noradrenergic nerve terminals originating in the LC, which has a robust GAL/GMAP synthesis. The functional role of GAL may be related to noradrenaline, possibly by a presynaptic action. However, the presence of GAL in other systems and of GAL-R2 receptor mRNA in granule cells also indicates other targets. J. Comp. Neurol. 392:227–251, 1998. © 1998 Wiley-Liss, Inc.The Journal of Comparative Neurology 03/1998; 392(2):227 - 251. DOI:10.1002/(SICI)1096-9861(19980309)392:2<227::AID-CNE6>3.0.CO;2-4 · 3.51 Impact Factor