RRC ID 170
Author Liu Y, Imai H, Sadamatsu M, Tsunashima K, Kato N.
Title Cytokines participate in neuronal death induced by trimethyltin in the rat hippocampus via type II glucocorticoid receptors.
Journal Neurosci. Res.
Abstract We investigated the role of IL-1alpha and IL-1beta expressed in the reactive gliosis following hippocampal damage induced by trimethyltin (TMT). IL-1alpha immunoreactivity was expressed earlier in small glial cells on day 4 post-TMT, while IL-1beta expression was obvious in large swollen glial cells on day 14 post-TMT. Both IL-1alpha and IL-1beta immunoreactivities were double-labeled with astrocyte marker, vimentin, but not with a microglia marker, OX-42. The expression of both IL-1alpha/beta was enhanced by adrenalectomy (ADX) prior to TMT administration. Corticosterone (CORT) or dexamethasone (DEX) supplementation not only cancelled effects of ADX, but also partially reversed TMT-induced enhancement of IL-1alpha/beta expressions. These changes coincided with TMT-induced neuronal death in CA3 pyramidal cells of the hippocampus. It is suggested that IL-1alpha/beta expressed in reactive astrocytes participate in TMT neurotoxicity via type II glucocorticoid receptors.
Volume 51(3)
Pages 319-27
Published 2005-3
PII S0168-0102(04)00309-8
PMID 15773051
MeSH Adrenalectomy Animals Anti-Inflammatory Agents / pharmacology Cell Death / drug effects Cell Death / physiology* Cortisone / pharmacology Cytokines / drug effects Cytokines / metabolism* Dexamethasone / pharmacology Gliosis / chemically induced Hippocampus / drug effects Hippocampus / pathology* Image Processing, Computer-Assisted Immunohistochemistry Infusion Pumps, Implantable Male Microscopy, Confocal Neuroglia / drug effects Neuroglia / metabolism Neurons / drug effects Neurons / pathology* Rats Receptors, Glucocorticoid / drug effects Receptors, Glucocorticoid / metabolism* Receptors, Glucocorticoid / physiology* Trimethyltin Compounds / toxicity*
IF 2.277