CLINICAL NEUROSCIENCE AND NEUROPATHOLOGYType C botulinum toxin causes degeneration of motoneurons in vivoZhao, Li-Chuna b; Yang, Boa; Wang, Renganga; Lipton, Stuart A.a; Zhang, DongxianaAuthor Information aCenter for Neuroscience, Aging and Stem Cell Research, Burnham Institute for Medical Research, La Jolla, California, USA bSchool of Pharmacy, Jilin University, Changchun, China Correspondence to Dr Dongxian Zhang, PhD, Center for Neuroscience, Aging and Stem Cell Research, Burnham Institute for Medical Research, La Jolla, CA 92037, USA Tel: +1 85 8795 5263; fax: +1 85 8795 5292; e-mail: firstname.lastname@example.org Li-Chun Zhao and Bo Yang contributed equally to this study Received 3 June 2009 accepted 12 July 2009 NeuroReport: January 6th, 2010 - Volume 21 - Issue 1 - p 14-18 doi: 10.1097/WNR.0b013e328330dcca Buy SDC Metrics Abstract All botulinum toxins (BoNTs, types A–G) inhibit synaptic transmitter release from motoneurons, and thus result in respiratory arrest and death. Rapid treatment with anti-BoNT antibodies can prevent progression, but recovery still requires weeks on a ventilator. Even after recovery, there is a potential for persistent fatigue in some cases of botulism even years after the insult, possibly because of motoneuron dropout for previously unknown reasons. Unique among BoNTs, the C-type (BoNT/C) cleaves two proteins involved in neurotransmitter release, syntaxin and SNAP-25, and induces apoptotic cell death in cultured cerebellar neurons. It is not clear, however, whether BoNT/C also affects neurons that encounter toxin in vivo, namely motoneurons. Here, we provide experimental evidence that BoNT/C causes a slow degeneration of motoneurons both in vitro and in vivo. This novel form of BoNT/C-induced cell death may require new treatment strategies. © 2010 Lippincott Williams & Wilkins, Inc.