Sweeney S T, Broadie K, Keane J, Niemann H, O'Kane C J
Department of Genetics, University of Cambridge, England.
Neuron. 1995 Feb;14(2):341-51. doi: 10.1016/0896-6273(95)90290-2.
Tetanus toxin cleaves the synaptic vesicle protein synaptobrevin, and the ensuing loss of neurotransmitter exocytosis has implicated synaptobrevin in this process. To further the study of synaptic function in a genetically tractable organism and to generate a tool to disable neuronal communication for behavioural studies, we have expressed a gene encoding tetanus toxin light chain in Drosophila. Toxin expression in embryonic neurons removes detectable synaptobrevin and eliminates evoked, but not spontaneous, synaptic vesicle release. No other developmental or morphological defects are detected. Correspondingly, only synaptobrevin (n-syb), but not the ubiquitously expressed syb protein, is cleaved by tetanus toxin in vitro. Targeted expression of toxin can produce specific behavioral defects; in one case, the olfactory escape response is reduced.
破伤风毒素可切割突触小泡蛋白突触结合蛋白，随后神经递质胞吐作用的丧失表明突触结合蛋白参与了这一过程。为了进一步研究基因易处理生物体中的突触功能，并生成一种用于行为研究中阻断神经元通讯的工具，我们在果蝇中表达了一种编码破伤风毒素轻链的基因。胚胎神经元中的毒素表达消除了可检测到的突触结合蛋白，并消除了诱发的而非自发的突触小泡释放。未检测到其他发育或形态缺陷。相应地，在体外只有突触结合蛋白（n-syb），而不是普遍表达的syb蛋白，会被破伤风毒素切割。毒素的靶向表达可产生特定的行为缺陷；在一个案例中，嗅觉逃避反应减弱。
