title: Acute injection of adrenal steroids reduces cornea-evoked expression of c-fos within the spinal trigeminal nucleus of adrenalectomized rats.
abstract: The influence of transient increases in adrenal steroid hormones on the number of Fos-positive neurons after nociceptor activation was assessed in adrenalectomized rats. Fos protein, the product of the immediate early gene, c-fos, was detected immunocytochemically within the spinal trigeminal nucleus 2 h after noxious thermal stimulation of the cornea. Adrenalectomized rats displayed an enhanced number of Fos-positive neurons within the caudal-most portions of trigeminal subnucleus caudalis compared to that seen in adrenal-intact animals, an effect reversed by a single acute injection of corticosterone (1 mg/kg, i.p.) given 5 min prior to stimulation. Acute injection of the selective mineralocorticoid receptor agonist, aldosterone, or the selective glucocorticoid receptor agonist, RU28362, also reduced the number of Fos-positive neurons. Aldosterone and RU28362 had an additive effect on Fos when given concurrently. In contrast, adrenal status or acute injections of adrenal steroid receptor agonists had no effect on the number of Fos-positive neurons after corneal stimulation located within the ventrolateral pole of the spinal trigeminal nucleus at the level of the subnucleus interpolaris/caudalis junction. Acute administration of adrenal steroids to adrenalectomized rats greatly attenuated the number of Fos-positive neurons seen after corneal stimulation within select portions of trigeminal subnucleus caudalis. The contribution of both glucocorticoid and mineralocorticoid receptor subtypes in reducing Fos suggested a central site of action rather than an anti-inflammatory effect on peripheral tissue. These results are consistent with the hypothesis that transient increases in adrenal steroids, such as occur after injury, are sufficient to modify the production of Fos protein in central neurons that process nociceptive information.
authors.affiliation: Department of Neuroscience, Brown University/Rhode Island Hospital, Providence 02903, USA.
authors.forename: J
authors.initials: J
authors.lastname: Lu
authors.forename: D A
authors.initials: DA
authors.lastname: Bereiter
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000315:Adrenalectomy; D000732:Androstanols / Q000494:pharmacology; D000818:Animals; D003315:Cornea; D015870:Gene Expression; D007150:Immunohistochemistry; D008297:Male; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis* / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D014279:Trigeminal Nucleus, Spinal / Q000187:drug effects*
chemical_list: D000305:Adrenal Cortex Hormones; D000732:Androstanols; D016760:Proto-Oncogene Proteins c-fos; C049154:11,17-dihydroxy-6-methyl-17-(1-propynyl)androsta-1,4,6-triene-3-one