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

We investigated the role of IL-1α and IL-1β expressed in the reactive gliosis following hippocampal damage induced by trimethyltin (TMT). IL-1α immunoreactivity was expressed earlier in small glial cells on day 4 post-TMT, while IL-1β expression was obvious in large swollen glial cells on day 14 post-TMT. Both IL-1α and IL-1β immunoreactivities were double-labeled with astrocyte marker, vimentin, but not with a microglia marker, OX-42. The expression of both IL-1α/β 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-1α/β expressions. These changes coincided with TMT-induced neuronal death in CA3 pyramidal cells of the hippocampus. It is suggested that IL-1α/β expressed in reactive astrocytes participate in TMT neurotoxicity via type II glucocorticoid receptors.