Bolon B, St Omer V E
Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia 65211.
Neurosci Biobehav Rev. 1992 Summer;16(2):171-5. doi: 10.1016/s0149-7634(05)80178-2.
Humoral signals (neurotransmitters and hormones) control cell division, migration, and differentiation processes which define the organization of brain pathways. Alterations in maternal, fetal, and neonatal biochemistry during critical periods of neurogenesis may irreparably alter the circuitry and, thus, postnatal behavior of young animals. Secalonic acid D (SAD), an ergochrome mycotoxin, causes behavioral and neurochemical deficits in developing mice following prenatal (transplacental) or early postnatal (transmammary) exposure. SAD-induced functional abnormalities include delays in reflex behaviors, integrated neuromuscular activity and strength, stress adaptation responses, and sensory discrimination. These behavioral changes are associated with reductions of brain monoamine neurotransmitter levels in both fetuses and neonates. SAD also alters concentrations of maternal plasma corticosteroids and fetal cyclic nucleotides during midgestation. SAD thus modulates several chemicals in pregnant mice and their fetuses which contribute to brain development, suggesting that this mycotoxin may pose a neuroteratogenic hazard to other immature mammals, including human infants.
体液信号（神经递质和激素）控制着细胞分裂、迁移和分化过程，这些过程决定了脑通路的组织形式。在神经发生的关键时期，母体、胎儿和新生儿的生物化学变化可能会对幼小动物的神经回路以及出生后的行为造成不可挽回的改变。色二酮酸D（SAD）是一种麦角色素真菌毒素，在产前（经胎盘）或产后早期（经乳腺）接触后，会导致发育中的小鼠出现行为和神经化学缺陷。SAD诱导的功能异常包括反射行为延迟、神经肌肉综合活动和力量、应激适应反应以及感觉辨别能力下降。这些行为变化与胎儿和新生儿脑单胺神经递质水平降低有关。SAD还会在妊娠中期改变母体血浆皮质类固醇和胎儿环核苷酸的浓度。因此，SAD会调节妊娠小鼠及其胎儿体内几种有助于大脑发育的化学物质，这表明这种真菌毒素可能会对包括人类婴儿在内的其他未成熟哺乳动物构成神经致畸危害。
