美国科学家发现，孕妇饮用酒精会阻碍胎儿脑中一些神经元正常发育的分子路径，这些神经元负责感觉输入和运动控制。
饮用酒精的孕妇增加了“胎儿酒精谱系障碍”的风险，该障碍包括几个脑区域不正常发育，特别是小脑。小脑是发现ADNP 浓度最高的一个脑区域。ADNP是来自星型胶质细胞的蛋白质，已知可以促进轴突和树突的生长并保护神经元不受伤害，包括不受乙醇的伤害。
美国哈佛医学院Suzhen Chen和Michael Charness发现乙醇抑制了ADNP对神经发育的积极影响。这组作者发现，仅仅10mM浓度的乙醇就阻止了神经元的生长——女性在饮用仅仅两杯酒精饮料之后1小时就能达到这个浓度。这组科学家对培养的小脑神经元进行了实验，从而证明ADNP促进的生长需要“Fyn激酶”的作用，这是一种信号传导分子，它能启动神经元长长的连接部分也就是轴突的生长。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS，vol. 105 no. 46 17867-17871，Suzhen Chen ，Michael E. Charness
Ethanol inhibits neuronal differentiation by disrupting activity-dependent neuroprotective protein signaling
Suzhen Chen and Michael E. Charness1
VA Boston Healthcare System, 1400 VFW Parkway, West Roxbury, MA 02132; and Department of Neurology, Harvard Medical School, Boston, MA 02115
Abstract
The mechanisms by which ethanol damages the developing and adult central nervous system (CNS) remain unclear. Activity-dependent neuroprotective protein (ADNP) is a glial protein that protects the CNS against a wide array of insults and is critical for CNS development. NAPVSIPQ (NAP), a potent active fragment of ADNP, potentiated axon outgrowth in cerebellar granule neurons by activating the sequential tyrosine phosphorylation of Fyn kinase and the scaffold protein Crk-associated substrate (Cas). Pharmacological inhibition of Fyn kinase or expression of a Fyn kinase siRNA abolished NAP-mediated axon outgrowth. Concentrations of ethanol attained after social drinking blocked NAP-mediated axon outgrowth (IC50 = 17 mM) by inhibiting NAP activation of Fyn kinase and Cas. These findings identify a mechanism for ADNP regulation of glial–neuronal interactions in developing cerebellum and a pathogenesis of ethanol neurotoxicity.
