1,720,962 research outputs found
Acute and chronic effects of the pesticide amitraz on α2-adrenoceptors in the mouse brain
No full textThere is increasing evidence to suggest that several effects of the formamidine pesticide amitraz (AMZ) in mammals are mediated by its interaction with α2-adrenoceptors. AMZ has been shown to inhibit the binding of [3H]clonidine, a specific ligand for α2-adrenoceptors to mouse brain in vitro and after administration in vivo. In the present study we have further investigated and characterized the effects of acute and chronic administration of AMZ on brain α2-adrenoceptors in mice. AMZ caused a dosedependent inhibition of [3H]clonidine binding. This inhibition was long-lasting (more than 48 h) following a relatively high dose of AMZ (75 mg/kg), while it was of short duration (2 h) following low doses (7.5 and 12.5 mg/kg). The time course of inhibition of [3H]clonidine binding was correlated with the plasma levels of AMZ and/or its active metabolites, measured with a novel radioreceptor binding technique. The alteration of [3H]clonidine binding was due to a decrease in α2-adrenoceptor affinity, with no change in the density of binding sites, and was reversible in vitro upon repeated washing of the membrane preparation. Repeated administration of 7.5 mg/kg or 12.5 mg/kg AMZ, to yield a total dose of 75 mg/kg, showed no evidence of a cumulative effect on brain α2-adrenoceptors. © 1989
Alpha 2-adrenoceptors as a target for formamidine pesticides: in vitro and in vivo studies in mice
No full textWhile the toxicity in insects of formamidines such as chlordimeform (CDM), its demethylated metabolite DCDM, and amitraz (AMZ) appears to involve activation of an octopamine-sensitive adenylate cyclase, their mechanism of action in mammals remains elusive. There is increasing evidence, however, that alpha 2-adrenoceptors might mediate certain effects of CDM, DCDM, and AMZ. In the present study, we investigated whether formamidines can interact directly with adrenoceptors in mouse forebrain both in vitro and after in vivo administration. Formamidines were potent inhibitors of the binding of [3H]clonidine to alpha 2-adrenoceptors with IC50's of 13 microM, 29 nM, and 130 nM for CDM, DCDM, and AMZ, respectively. Binding of [3H]yohimbine was inhibited with similar potencies. All compounds also inhibited with equal (CDM) or lower potency the binding of [3H]spiperone to dopamine D2 receptors and were weak inhibitors or inactive toward alpha 1- and beta-adrenoceptors, cholinergic muscarinic, GABAA, opiate mu, benzodiazepine, and histamine 1 receptors. Administration of formamidines to mice caused a dose-dependent decrease of [3H]clonidine binding. [3H]Clonidine binding returned to control values within 5 hr following administration of CDM and DCDM, but was still significantly decreased up to 48 hr after AMZ. Among different brain regions, [3H]clonidine binding was decreased to a larger extent in cerebral cortex, hippocampus, and midbrain. In vitro and ex vivo kinetic binding studies indicated that the effect of formamidines on alpha 2-adrenoceptors was due to a decrease in affinity and not to an alteration of the density of [3H]clonidine binding sites. The results of these biochemical studies support the hypothesis that alpha 2-adrenoceptors represent an important target for formamidine neurotoxicity in mammals
Vigabatrin does not effect the intestinal absorption of phenytoin in rat duodeno-jejunal loops in situ.
No full textIn this study, an in situ rat intestinal loop model was use to examine the effect of vigabatrin on the intestinal absoprtion of phenytoin
Neurological deficit following spinal anaesthesia: MRI and CT evidence of spinal cord gas embolism.
No full textA 62-year-old diabetic woman developed permanent neurological deficits in the legs following spinal anaesthesia. MRI showed oedema in the spinal cord and a small intramedullary focus of signal void at the T10 level, with negative density at CT. Intramedullary gas bubbles have not been reported previously among the possible neurological complications of spinal anaesthesia; a combined ischaemic/embolic mechanism is hypothesised
Formamidine pesticides and alpha 2-adrenoceptors: studies with amitraz and chlordimeform in rats and development of a radioreceptor binding assay
No full textThe interaction of the formamidine pesticides chlordimeform (CDM) and amitraz (AMZ) with rat brain alpha2-adrenoceptors was investigated. Both compounds inhibited the binding of 3H-clonidine and 3H-yohimbine in vitro with IC50 values of 62-68 microM (CDM) and 95-110 nM (AMZ). In vivo administration of AMZ and CDM caused a dose-dependent inhibition of 3H-clonidine binding in rat forebrain. The inhibition was short-lasting (24 hr) following CDM administration, while after AMZ recovery of 3H-clonidine binding occurred only after 72 hr. Good correlations were found between inhibition of brain 3H-clonidine binding by the formamidines and "plasma equivalents" of these compounds and/or their biologically active metabolites, as measured by a new radioreceptor assay. These results suggest that 1) formamidines can interact in vivo with brain alpha 2-adrenoceptors when administered at doses previously shown to cause toxic effects on the central nervous system: and 2) this effect is reversible, both in vivo and in vitro, and appears to be linked to the presence of the formamidines and/or their active metabolites at the receptor sites
Acute and chronic effects of the pesticide amitraz on alpha 2-adrenoceptors in mouse brain
No full textThere is increasing evidence to suggest that several effects of the formamidine pesticide amitraz (AMZ) in mammals are mediated by its interaction with alpha 2-adrenoceptors. AMZ has been shown to inhibit the binding of [3H]clonidine, a specific ligand for alpha 2-adrenoceptors to mouse brain in vitro and after administration in vivo. In the present study we have further investigated and characterized the effects of acute and chronic administration of AMZ on brain alpha 2-adrenoceptors in mice. AMZ caused a dose-dependent inhibition of [3H]clonidine binding. This inhibition was long-lasting (more than 48 h) following a relatively high dose of AMZ (75 mg/kg), while it was of short duration (2 h) following low doses (7.5 and 12.5 mg/kg). The time course of inhibition of [3H]clonidine binding was correlated with the plasma levels of AMZ and/or its active metabolites, measured with a novel radioreceptor binding technique. The alteration of [3H]clonidine binding was due to a decrease in alpha 2-adrenoceptor affinity, with no change in the density of binding sites, and was reversible in vitro upon repeated washing of the membrane preparation. Repeated administration of 7.5 mg/kg or 12.5 mg/kg AMZ, to yield a total dose of 75 mg/kg, showed no evidence of a cumulative effect on brain alpha 2-adrenoceptors
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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