Assuntos
Otopatias/etiologia , Herpes Zoster/complicações , Animais , Cricetinae , Otopatias/microbiologia , Orelha Externa/microbiologia , Paralisia Facial/etiologia , Paralisia Facial/microbiologia , Feminino , Transtornos da Audição/etiologia , Transtornos da Audição/microbiologia , Humanos , Masculino , Pessoa de Meia-Idade , Síndrome , Nervo Vestibulococlear/microbiologiaRESUMO
The action of 1.0 and 10.0 mg/kg (i.p.) of corticosterone on serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) contents and on serotonin turnover, measured by an MAO-inhibitor method, was studied at 30 and 120 min after administration. A 1.0 mg/kg dose of corticosterone increased the serotonin content and turnover in the hypothalamus and mesencephalon 30 min after administration; however, it was ineffective on dorsal hippocampus and frontal and parietal cortex. 5-HIAA content did not change significantly in any of the brain areas studied. A 10.0 mg/kg dose of corticosterone decreased the serotonin content and turnover in the hypothalamus and mesencephalon; it was ineffective in other brain areas investigated. 5-HIAA content significantly decreased in the hypothalamus while it increased in the mesencephalon and dorsal hippocampus. In the parietal and frontal cortex, 5-HIAA content did not change following administration of 10.0 mg/kg of corticosterone. At 120 min after corticosterone administration, neither 5-HT content and turnover nor 5-HIAA content showed any change in the brain areas investigated. The results suggest that corticosteroids might change the activity of the brain serotoninergic system in a dose- and time-dependent manner, and in this way the serotoninergic system might play an important role in mediation of the corticosteroid effect exerted on brain function.
RESUMO
Electric stimulation of rat midbrain raphe nuclei by means of chronically implanted bipolar electrodes was able to reduce the stress-induced increase in plasma corticosterone level by about 40-50%. A serotonin receptor blocker, methysergide, prevented the stimulation-induced inhibition of the stress response. The results support the possible existence of serotoninergic inhibition of hypothalamo-pituitary-adrenocortical activation in rats.