Lelyanova V G, Thomson D, Ribchester R R, Tonevitsky E A, Ushkaryov Y A
Department of Cell and Molecular Biology, Imperial College, London, U.K.
Bull Exp Biol Med. 2009 Jun;147(6):701-3. doi: 10.1007/s10517-009-0600-5.
The mechanisms of acetylcholine release in presynaptic terminals of motoneurons induced by mutant alpha-latrotoxin (LT(N4C)) were analyzed. In contrast to wild-type alpha-latrotoxin that causes both continuous and splash secretion of acetylcholine and necessarity block neuromuscular transmission, LT(N4C) causes only splash release lasting over many hours. Thus, activation of alpha-latrotoxin receptors controls long-lasting enhanced secretion of acetylcholine.
分析了突变型α-黑寡妇毒素（LT(N4C)）诱导运动神经元突触前终末释放乙酰胆碱的机制。与导致乙酰胆碱持续和飞溅式分泌并必然阻断神经肌肉传递的野生型α-黑寡妇毒素不同，LT(N4C)仅引起持续数小时的飞溅式释放。因此，α-黑寡妇毒素受体的激活控制着乙酰胆碱的长期增强分泌。
