Siegel L S, Price J I
Pathology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21701.
Toxicon. 1987;25(9):1015-8. doi: 10.1016/0041-0101(87)90166-8.
Clostridium botulinum neurotoxins inhibit acetylcholine release at neuromuscular junctions. Agents stimulating neurotransmitter efflux, such as 3,4-diaminopyridine (3,4-DAP), could be useful for botulism therapy. Treatment with 3,4-DAP (8 mg/kg hourly, beginning 3 hr after toxin injection) failed to increase the survival times of mice receiving 10, 20 or 40 LD50 type C, but did prolong the survival of those receiving 20 LD50 type A. This difference in 3,4-DAP efficacy may reflect variations in the molecular mechanism of action of types A and C botulinum neurotoxins.
肉毒梭菌神经毒素可抑制神经肌肉接头处乙酰胆碱的释放。刺激神经递质外流的药物,如3,4-二氨基吡啶(3,4-DAP),可能对肉毒中毒治疗有用。用3,4-DAP治疗(每小时8毫克/千克,在毒素注射后3小时开始)未能延长接受10、20或40个C型半数致死量(LD50)的小鼠的存活时间,但确实延长了接受20个A型LD50的小鼠的存活时间。3,4-DAP疗效的这种差异可能反映了A型和C型肉毒梭菌神经毒素作用分子机制的差异。