Rapidly activated microglial cells in the preoptic area may play a role in the generation of hyperthermia following occlusion of the middle cerebral artery in the rat.

Abstract

Postischemic hyperthermia occurs after the occlusion of the middle cerebral artery (MCAO) with an intraluminal filament in rats. The cause of hyperthermia is presumed to be damage to the preoptic area, which is one of the temperature-regulatory centers of the hypothalamus. In the present study, reactions of microglial cells and astrocytes in the preoptic area were examined during the first 6 h following transient MCAO. Microglial cells and astrocytes were visualized with immunohistochemistry using antibodies against the CR3 complement receptor and the glial fibrillary acidic protein, respectively. One hour after the occlusion, activated microglial cells were observed in both the medial and lateral preoptic areas ipsilaterally, and in the medial preoptic area contralateral to the infarct. Following reperfusion, the activation of microglial cells decreased in the medial preoptic area of both hemispheres, and in the lateral preoptic area there was a loss of immunoreactive microglial cells. Fragmentation of astrocytic processes was detected in the lateral preoptic area, while in the ipsilateral medial preoptic area a moderate swelling was observed. Immunohistochemistry with an antibody against interleukin-1beta (IL-1beta) revealed scattered immunoreactive cells in both the ipsilateral and the contralateral medial preoptic area 2 h after the MCAO. Our results show that microglial activation in the preoptic area coincides with postischemic hyperthermia. However, an exclusive role for IL-1beta in the generation of hyperthermia is unlikely, and other factors are probably also responsible for postischemic hyperthermia.