Cytokines participate in neuronal death induced by trimethyltin in the rat hippocampus via type II glucocorticoid receptors

Neurosci Res. 2005 Mar;51(3):319-27. doi: 10.1016/j.neures.2004.12.005.

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.

Publication types

  • Corrected and Republished Article

MeSH terms

  • 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*

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Receptors, Glucocorticoid
  • Trimethyltin Compounds
  • Dexamethasone
  • Cortisone