• Neuroscience · Aug 2017

    Antinociceptive effect of botulinum toxin A involves alterations in AMPA receptor expression and glutamate release in spinal dorsal horn neurons.

    • Bin Hong, LingLing Yao, Linhui Ni, Li Wang, and XingYue Hu.
    • Neurology Department of Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, China. Electronic address: hongbin@zju.edu.cn.
    • Neuroscience. 2017 Aug 15; 357: 197-207.

    AbstractThe use of botulinum toxin A (BTX-A) for various clinical therapeutic applications is increasing. It is widely believed that peripheral therapeutic or toxic effects of BTX-A are exclusively mediated by SNAP-25 cleavage. There is growing evidence of long-distance retrograde axonal transport of BTX-A on entering the central nervous system, subsequent to a local injection of the toxin. However, the prevalence of central antinociceptive effects after BTX-A peripheral application and its underlying mechanisms are unclear. Our results show that (1) BTX-A can undergo retrograde axonal transport to the dorsal horn after peripheral application; (2) Peripheral pretreatment with BTX-A decreases the expression and function of AMPA receptors in the spinal cord dorsal horn neurons; (3) Peripheral pretreatment with BTX-A does not change basal glutamate release, but decreases the effect of formalin-evoked release of glutamate in spinal cord dorsal horn neurons. These results suggest that peripheral application of BTX-A can change AMPA receptor expression in, and glutamate release from, spinal dorsal horn neurons, which may have significance in its central antinociceptive effects.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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