{"title":"Influence of hormones and hormone antagonists on sexual differentiation of the brain.","authors":"K D Döhler","doi":"10.1007/978-3-642-46856-8_12","DOIUrl":null,"url":null,"abstract":"<p><p>In summary, a number of studies have shown that not only estrogenic and androgenic steroids and their antagonists influence sexual differentiation of the mammalian brain but also drugs which stimulate or inhibit the adrenergic, the serotoninergic, or the cholinergic system in the developing brain. The present knowledge on the possible participation of neurotransmitter systems in sexual differentiation of the brain and their mode of interaction in this process perinatally with gonadal steroids is still rather limited. Sexual differentiation of the central nervous system is a complex integrated process, which relies on proper chronological and quantitative interactions of various endocrine and neuroendocrine mediators. Any disturbance of this delicate endogenous hormonal balance during ontogenetic development, e.g. by means of environmental influences, can result in permanent manifestation of anatomic and functional sexual deviations. A large number of man-made chemicals that have been released into the environment have the potential to disrupt the endocrine system of animals and humans. They do so because they mimick the effects of natural hormones or neurotransmitters by recognizing their binding sites, or they antagonize the effects of endogenous hormones or neurotransmitters by blocking their interaction with their physiological binding sites. Interaction of environmental endocrine disruptors with animals or humans during ontogeny may have deleterious effects on the differentiation of reproductive structures and functions, rendering the individuals in question permanently incapable to reproduce and, thus, endangering survival of the species.</p>","PeriodicalId":8353,"journal":{"name":"Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement","volume":"20 ","pages":"131-41"},"PeriodicalIF":0.0000,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"28","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-642-46856-8_12","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 28
Abstract
In summary, a number of studies have shown that not only estrogenic and androgenic steroids and their antagonists influence sexual differentiation of the mammalian brain but also drugs which stimulate or inhibit the adrenergic, the serotoninergic, or the cholinergic system in the developing brain. The present knowledge on the possible participation of neurotransmitter systems in sexual differentiation of the brain and their mode of interaction in this process perinatally with gonadal steroids is still rather limited. Sexual differentiation of the central nervous system is a complex integrated process, which relies on proper chronological and quantitative interactions of various endocrine and neuroendocrine mediators. Any disturbance of this delicate endogenous hormonal balance during ontogenetic development, e.g. by means of environmental influences, can result in permanent manifestation of anatomic and functional sexual deviations. A large number of man-made chemicals that have been released into the environment have the potential to disrupt the endocrine system of animals and humans. They do so because they mimick the effects of natural hormones or neurotransmitters by recognizing their binding sites, or they antagonize the effects of endogenous hormones or neurotransmitters by blocking their interaction with their physiological binding sites. Interaction of environmental endocrine disruptors with animals or humans during ontogeny may have deleterious effects on the differentiation of reproductive structures and functions, rendering the individuals in question permanently incapable to reproduce and, thus, endangering survival of the species.