Long-term maternal 2,3,7,8-Tetrachlorodibenzo-p-dioxin altered neuronal activities of brains of mouse offspring

点击翻译按钮获取中文摘要

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic environment contaminants. Acute administration of a lethal dose of TCDD to adult animals induces a variety of severe intoxication effects. Although penetration of TCDD into the brain is poor, it is still detected in the brain with higher concentrations in the hypothalamus. However, little direct morphological evidence clarifying whether the central nervous system (CNS) is involved in the TCDD-induced intoxication. Fos protein, a product of the immediate-early gene c-Fos, is generally considered to be a specific marker of neuronal activation. The present study was conducted to examine the c-Fos expression patterns in the CNS following administration of a single lethal dose of TCDD to the adult Long-Evans rat.On the other hand, TCDD is transferred to each fetus and pup transplacentally and lactationally, and it produces a wide variety of toxic effects in offspring. The CNS during early development may also be a potential target of TCDD. Previous study suggested that dopaminergic neurons of male non-human primates at least were targets of dioxin toxicity, and we examined serotonin-immunoreactive neurons in the raphe nuclei of male offspring of ddY mouse exposed to TCDD in utero and via lactation. Labeled neurons were similarly distributed in the raphe nuclei. However, a marked decrease in intensity of immunostaining occurred in all raphe nuclei, and consequently, the detectable serotonin-immunoreactive neurons were greatly decreased in number. The decreases in staining intensity occurred almost uniformly in each raphe subnucleus, the dorsal raphe nucleus, median raphe nucleus, supralemniscal area, nucleus raphe magnus.