Circulating Corticosterone Alters the Rate of Neuropathological and Behavioral Changes Induced by Trimethyltin in Rats

Tsutsumi, Shunsuke; Akiyama, Masashi; Arimitsu, H.; Imai, Hideki; Kato, Nobuo

doi:10.1006/exnr.2001.7824

Cited by 21 publications

(13 citation statements)

References 27 publications

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“…11 A consistently reported consequence of TMT exposure has been hyperactivity observed in the openfield. 12,13 The results of the present study confirm these observations and also address the time-dependent nature of the phenomenon.…”

Section: Open Field Test (Oft)supporting

confidence: 89%

Grafts containing human amniotic epithelial cells reduce hyperactivity in open-field and digital photo-actometer after Trimethyltin chloride lesion

Omprakash

Muthusamy

Devanand

et al. 2010

Journal of Institute of Medicine

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Section: Open Field Test (Oft)supporting

confidence: 89%

Grafts containing human amniotic epithelial cells reduce hyperactivity in open-field and digital photo-actometer after Trimethyltin chloride lesion

Omprakash

Muthusamy

Devanand

et al. 2010

Journal of Institute of Medicine

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“…Evidence for this idea comes from the earlier findings that TMT treatment produces an increase in plasma corticosterone (14) and that metyrapone, an inhibitor of corticosterone synthesis, has the ability to improve TMT-induced neuronal damage in the hippocampus of rats (15). Paradoxically, it was also reported that TMT neurotoxicity is exacerbated by adrenalectomy, which is followed by depletion of endogenous corticosterone, and that dexamethasone, an agonist for glucocorticoid receptors (type II corticosterone receptors), is effective in alleviating TMT neurotoxicity in rats (16).…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the finding that an acute treatment with TMT temporally increases the concentration of plasma corticosterone in rats (14), it has been demonstrated that a reduction in the level of circulating corticosterone by metyrapone, an inhibitor of corticosterone synthesis, prevents TMT from damaging the hippocampal neurons and eliciting learning impairment and hyperactivity in rats (15). Contrariwise, there exists an opposing report indicating that in adrenalectomized (ADX) rats, the depletion of circulating corticosterone facilitates TMTinduced damage to CA3 pyramidal cells of the hippocampus (16).…”

Section: Introductionmentioning

confidence: 99%

Endogenous and Exogenous Glucocorticoids Prevent Trimethyltin From Causing Neuronal Degeneration of the Mouse Brain In Vivo: Involvement of Oxidative Stress Pathways

et al. 2009

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Abstract. The organotin trimethyltin (TMT) is known to cause neuronal degeneration in the murine brain. Earlier studies indicate that TMT-induced neuronal degeneration is enhanced by adrenalectomy. However, no evaluation has been attempted to determine the mechanism underlying the enhancement of TMT neurotoxicity by adrenalectomy and its implications in neuronal degeneration. To assess the implications and determine the mechanism of adrenalectomyelicited enhancement of TMT neurotoxicity, we examined neuronal degeneration and associated signaling pathways in adrenalectomized mice. Adrenalectomy dramatically enhanced the TMTinduced neuronal damage in certain brain regions including the dentate gyrus, olfactory bulb, and anterior olfactory nucleus, in addition to exacerbating the behavioral abnormalities. TMTinduced activation of caspase-3 and calpain was also enhanced by adrenalectomy. The above events elicited by TMT were almost entirely prevented by treatment with dexamethasone. In addition to the above events, adrenalectomy clearly enhanced the activation of c-Jun-N-terminal kinases and the formation of 4-hydroxynonenal in the dentate gyrus following TMT treatment. The dentate granule cell damage induced by TMT was exacerbated by mifepristone, a glucocorticoid-receptor antagonist. Taken together, our data suggest that endogenous and exogenous glucocorticoids prevent neurodegeneration induced by TMT in the central nervous system by attenuating intensive oxidative stress and associated signaling pathways.

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“…Metyrapone, an inhibitor of corticosteroid synthesis, not only improved TMT-induced damage in the hippocampus, but also alleviated TMT-induced learning impairment as well as hyperactivity (Tsutsumi et al, 2002). Thus, TMT-induced neurotoxicity may be associated with the altered function of hypothalamo-pituitary-adrenocortical axis, since the hippocampus contains the highest density of corticosteroid receptors in the central nervous system (McEwen et al, 1968).…”

Section: Trimethyltinmentioning

confidence: 97%

Neurotoxins and neurotoxic species implicated in neurodegeneration

Segura‐Aguilar

Kostrzewa

2004

neurotox res

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Neurotoxins, in the general sense, represent novel chemical structures which when administered in vivo or in vitro, are capable of producing neuronal damage or neurodegeneration--with some degree of specificity relating to neuronal phenotype or populations of neurons with specific characteristics (i.e., receptor type, ion channel type, astrocyte-dependence, etc.). The broader term 'neurotoxin' includes this categorization but extends the term to include intra- or extracellular mediators involved in the neurodegenerative event, including necrotic and apoptotic factors. Moreover, as it is recognized that astrocytes are essential supportive satellite cells for neurons, and because damage to these cells ultimately affects neuronal function, the term 'neurotoxin' might reasonably be extended to include those chemical species which also adversely affect astrocytes. This review is intended to highlight developments that have occurred in the field of 'neurotoxins' during the past 5 years, including MPTP/MPP+, 6-hydroxydopamine (6-OHDA), methamphetamine; salsolinol; leukoaminochrome-o-semiquinone; rotenone; iron; paraquat; HPP+; veratridine; soman; glutamate; kainate; 3-nitropropionic acid; peroxynitrite anion; and metals (copper, manganese, lead, mercury). Neurotoxins represent tools to help elucidate intra- and extra-cellular processes involved in neuronal necrosis and apoptosis, so that drugs can be developed towards targets that interrupt the processes leading towards neuronal death.

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Circulating Corticosterone Alters the Rate of Neuropathological and Behavioral Changes Induced by Trimethyltin in Rats

Cited by 21 publications

References 27 publications

Grafts containing human amniotic epithelial cells reduce hyperactivity in open-field and digital photo-actometer after Trimethyltin chloride lesion

Grafts containing human amniotic epithelial cells reduce hyperactivity in open-field and digital photo-actometer after Trimethyltin chloride lesion

Endogenous and Exogenous Glucocorticoids Prevent Trimethyltin From Causing Neuronal Degeneration of the Mouse Brain In Vivo: Involvement of Oxidative Stress Pathways

Neurotoxins and neurotoxic species implicated in neurodegeneration

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