Marsal J, Solsona C, Rabasseda X, Blasi J
Departament de Biologia Cel-lular i Anatomia Patológica, Facultat de Medicina, Hospital de Bellvitge, Universitat de Barcelona, Barcelona, Catalonia, Spain.
Neurochem Int. 1988;12(4):439-45. doi: 10.1016/0197-0186(88)90026-5.
In previous reports, we have shown that botulinum neurotoxin inhibits acetylcholine release from Torpedo marmorata electric organ and from its synaptosomal fraction. Here, we have focussed our attention on the study of the effect of botulinum neurotoxin on the metabolism of acetylcholine, namely, the precursors supply, the synthesis activity and the storage of the neurotransmitter into nerve endings isolated from Torpedo electric organ. Radiolabelled acetylcholine precursors (acetate and choline) uptake, choline O-acetyltransferase activity, and the compartmentalization of the transmitter into the synaptosomes were not modified by botullinum neurotoxin. When labelled nerve ending were depolarized by K(+), the specific radioactivity of acetylcholine in the free pool fell markedly, but the specific radioactivity in the bound pool remained constant. Botulinum neurotoxin prevented this K(+)-induced decrease of specific radioactivity in the free pool.
在先前的报告中，我们已经表明肉毒杆菌神经毒素会抑制电鳐电器官及其突触体组分释放乙酰胆碱。在此，我们将注意力集中在研究肉毒杆菌神经毒素对乙酰胆碱代谢的影响上，即神经递质的前体供应、合成活性以及其在从电鳐电器官分离出的神经末梢中的储存。放射性标记的乙酰胆碱前体（乙酸盐和胆碱）摄取、胆碱O-乙酰转移酶活性以及递质在突触体中的分隔并未因肉毒杆菌神经毒素而改变。当标记的神经末梢被K(+)去极化时，游离池中乙酰胆碱的比放射性显著下降，但结合池中比放射性保持恒定。肉毒杆菌神经毒素阻止了游离池中这种由K(+)诱导的比放射性下降。
