美國科學家發(fā)現(xiàn),，孕婦飲用酒精會阻礙胎兒腦中一些神經(jīng)元正常發(fā)育的分子路徑，這些神經(jīng)元負責感覺輸入和運動控制,。
飲用酒精的孕婦增加了“胎兒酒精譜系障礙”的風險,，該障礙包括幾個腦區(qū)域不正常發(fā)育,，特別是小腦,。小腦是發(fā)現(xiàn)ADNP 濃度最高的一個腦區(qū)域。ADNP是來自星型膠質細胞的蛋白質，已知可以促進軸突和樹突的生長并保護神經(jīng)元不受傷害,，包括不受乙醇的傷害,。
美國哈佛醫(yī)學院Suzhen Chen和Michael Charness發(fā)現(xiàn)乙醇抑制了ADNP對神經(jīng)發(fā)育的積極影響。這組作者發(fā)現(xiàn),，僅僅10mM濃度的乙醇就阻止了神經(jīng)元的生長——女性在飲用僅僅兩杯酒精飲料之后1小時就能達到這個濃度,。這組科學家對培養(yǎng)的小腦神經(jīng)元進行了實驗，從而證明ADNP促進的生長需要“Fyn激酶”的作用,，這是一種信號傳導分子,，它能啟動神經(jīng)元長長的連接部分也就是軸突的生長。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
