title: Corticosteroids limit microglial activation occurring during acute stress.
abstract: Our previous studies demonstrated that exposure of animals to acute stress immediately induced morphological microglial activation in the brain. Here we investigated the effects of adrenal corticoids on microglial activation following acute stress. We compared microglial activation in vivo in adrenalectomized (ADX), Sham-operated (SHM), and adrenalectomy plus corticosterone (CORT) administered rats exposed to a 2-h period of acute water restraint stress. We found that: (1) acute stress induced microglial activation in SHM rats; (2) acute stress robustly enhanced microglial activation in ADX rats; (3) CORT treatment significantly reduced the effects of adrenalectomy. Thus, while acute stress has the ability to activate microglia, the magnitude of activation is negatively regulated by CORT. Glucocorticoids may serve as an important endogenous suppressive signal limiting neuroinflammation that might otherwise occur during stress.
authors.affiliation: Department of Physiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. Electronic address: sugama@nms.ac.jp.
authors.forename: S
authors.initials: S
authors.lastname: Sugama
authors.affiliation: Division of Animal Sciences, National Institute of Agrobiological Sciences, Ohwashi 1-2, Tsukuba, Ibaraki 305-8634, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Takenouchi
authors.affiliation: Division of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156-0057, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Fujita
authors.affiliation: Division of Animal Sciences, National Institute of Agrobiological Sciences, Ohwashi 1-2, Tsukuba, Ibaraki 305-8634, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kitani
authors.affiliation: Department of Chemical Physiology, The Scripps Research Institute, 1055 North Torrey Pines Road, La Jolla, CA 92037, USA.
authors.forename: B
authors.initials: B
authors.lastname: Conti
authors.affiliation: Division of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156-0057, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hashimoto
mesh_terms: D000208:Acute Disease; D000315:Adrenalectomy; D000818:Animals; D002452:Cell Count; D048429:Cell Size; D003345:Corticosterone / Q000378:metabolism*; D005802:Genes, MHC Class II / Q000502:physiology; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D008297:Male; D017628:Microglia / Q000473:pathology / Q000502:physiology*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D017208:Rats, Wistar; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000473:pathology / Q000503:physiopathology*
chemical_list: D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D003345:Corticosterone