Comella J X, Molgo J, Faille L
Laboratoire de Neurobiologie Cellulaire et Moléculaire, Centre National de la Recherche Scientifique, Gif sur Yvette, France.
Neurosci Lett. 1993 Apr 16;153(1):61-4. doi: 10.1016/0304-3940(93)90077-x.
Paralysis of the mouse levator auris longus muscle by in vivo injection of Clostridium botulinum type-D neurotoxin (BoNT/D) triggered a marked outgrowth of the motor nerve from the original terminal arborization. The increase in total nerve terminal length was due to both increase in the number of terminal branches and in average branch length. Asynchronous quantal transmitter release in response to nerve impulses was a prominent feature in paralysed junctions that started 24 h after poisoning and lasted for about 15 days. The functional recovery of poisoned junctions occurred 25-30 days after poisoning and was characterized by the synchronous quantal transmitter release upon nerve stimulation that triggered synaptically evoked action potentials and muscle fibre contraction.
通过体内注射D型肉毒杆菌神经毒素（BoNT/D）使小鼠耳长提肌麻痹，引发了运动神经从原始终末分支显著长出。总神经末梢长度的增加是由于终末分支数量和平均分支长度均增加。中毒后24小时开始，瘫痪的神经肌肉接头处一个突出的特征是对神经冲动的异步量子递质释放，这种情况持续约15天。中毒的神经肌肉接头在中毒后25 - 30天出现功能恢复，其特征是神经刺激时量子递质同步释放，引发突触诱发动作电位和肌纤维收缩。
