Behavioral and immunohistochemical evidence for central antinociceptive activity of botulinum toxin A

摘要: Botulinum toxin A (BTX-A) is approved for treatment of different cholinergic hyperactivity disorders, and, recently, migraine headache. Although suggested to act only locally, novel observations demonstrated bilateral reduction pain after unilateral injection, and proposed retrograde axonal transport, presumably in sensory neurons. However, up now, transport BTX-A from periphery CNS was identified motoneurons, but with unknown significance. We assessed the effects low doses injected into rat whisker pad (3.5 U/kg) or trigeminal ganglion (1 on formalin-induced facial pain. Axonal prevented by colchicine injection (5 mM, 2 μl). To find possible site action axonally transported BTX-A, we employed immunohistochemical labeling BTX-A-truncated synaptosomal-associated protein 25 (SNAP-25) medullary dorsal horn nucleus caudalis pad. Both peripheral intraganglionic reduce phase II Antinociceptive effect completely colchicine. SNAP-25 (spinal nucleus) evident 3 days following treatment, even dose applied U/kg). Presented data provide first evidence that obligatory its antinociceptive effects, occurs via neurons directed nociceptive nuclei CNS.