Elevation of maternal glucocorticoid hormones alters neurotransmitter phenotypic expression in embryos.-猫眼课题宝

母体糖皮质激素的升高会改变胚胎中神经递质的表型表达。

DOI：

10.1016/0012-1606(81)90172-x

发表时间：

1981

期刊：

Developmental biology

影响因子：

2.7

通讯作者：

中科院分区：

生物学3区

文献类型：

作者：

G. Jonakait;M. Bohn;K. Markey;M. Goldstein;I. Black

越来越多的证据表明，母亲的经历可能会影响发育中的胚胎，特别是神经系统的发育。孕妇或哺乳期母亲暴露于抗精神病药物（通格，1973; Dailey，1978）、阿片类药物（Lau等人，1977）或利血平（Kovacic和罗宾逊，1966; Bartolome等，1976）与后代的神经和行为异常有关。此外，母体压力或升高母体糖皮质激素的治疗也可能导致神经缺陷（Barlow et al.，1978; Ward和Weisz，1980; Moyer等人，1978年）。导致这些发育缺陷的分子机制尚未确定。病理后遗症的神经递质表型表达异常的可能性仍然unexplored.We一直在研究影响神经递质表型的发展在一个假定的神经母细胞，位于胚胎大鼠肠道的人口的因素。该群体在正常妊娠期间瞬时表达许多去甲肾上腺素能表型特征（Cochard等人，1978，1979; Teitelman等人，1979年）。这些非常可塑的细胞为解决这些问题提供了一个有用的模型。该细胞群在妊娠第11.5天（E11）最初表现出儿茶酚胺（CA）荧光和对CA生物合成酶酪氨酸羟化酶（T-OH）和多巴胺-β-羟化酶（DBH）的免疫反应性。5; 27-30体节）（Cochard等人，1978，1979; Teitelman等人，1979年）。到E125（37-41体节），细胞数量增加并表达额外的去甲肾上腺素能特性：特异性高亲和力摄取去甲肾上腺素（NE; Jonakait et al.，1979年）。但在E13。5（48-50体节）内源CA和合成酶几乎完全消失。相反，NE摄取持续存在，表明

Increasing evidence suggests that maternal experience may affect the developing embryo in general, and the developing nervous system in particular. Exposure of pregnant or nursing mothers to antipsychotic agents (Tonge, 1973; Dailey, 1978), opiates (Lau et al., 1977), or reserpine (Kovacic and Robinson, 1966; Bartolome et al., 1976) is associated with neurologic and behavioral abnormalities in the offspring. Moreover, maternal stress or treatments which elevate maternal glucocorticoid hormones may also result in neurologic deficits (Barlow et al., 1978; Ward and Weisz, 1980; Moyer et al., 1978). The molecular mechanisms responsible for these developmental defects have yet to be defined. The possibility that pathologic sequelae derive from abnormalities in neurotransmitter phenotypic expression remains unexplored.We have been studying factors affecting the development of neurotransmitter phenotype in a population of presumptive neuroblasts, located in the embryonic rat gut. This population transiently expresses a number of noradrenergic phenotypic characters during normal gestation (Cochard et al., 1978, 1979; Teitelman et al., 1979). These remarkably plastic cells provide a useful model for addressing a number of these issues. This population of cells initially exhibits catecholamine (CA) fluorescence and immunoreactivity to the CA biosynthetic enzymes, tyrosine hydroxylase (T-OH) and dopamine-P-hydroxylase(DBH), on gestational Day 11.5 (E11. 5; 27-30 somites)(Cochard et al., 1978, 1979; Teitelman et al., 1979). By El25 (37-41 somites), the cells have increased in number and express an additional noradrenergic trait: the specific, high-affinity uptake of norepinephrine (NE; Jonakait et al., 1979). However, by E13. 5 (48-50 somites) endogenous CA and synthetic enzymes have almost completely disappeared. In contrast, NE uptake persists, suggesting that the

Translation of tyrosine hydroxylase from poly(A)-mRNA in pheochromocytoma cells is enhanced by dexamethasone.