At first merely a lethal toxin which causes botulism, BT-A has been successfully used for more than 30 years in the treatment of various ailments, of which chronic pain is an indication that continues to be researched. Though considered to be one of the most potent biological toxins, its purified pharmacological preparation BT-A in nanomolar doses is used in treating various clinical conditions accompanied by augmented muscular contractility. With regard to pain treatment, it offers a significant advantage – after a single administration, its effects persist for several months, which gives it an edge over popular analgesics, especially for chronic pain treatment. Previous research on visceral and bilateral pain models, which have shown a bilateral analgesic effect of BT-A after unilateral peripheral and intrathecal, but not central intracerebroventricular and intracisternal administration, has served as the foundation of the hypothesis on the central segmental analgesic effect of BT-A at the spinal level. Immunohistochemically detected cleaved SNAP-25 in the dorsal horn of the spinal cord indicates a retrograde axonal transport from the periphery to the spinal cord where it exhibits its antinociceptive effect by modulating pain impulse transmission via sensory fibers at the level of the first synapse in the spinal cord. This paper has immunohistochemically detected cleaved SNAP-25 in the dorsal horn of the spinal cord after the peripheral administration of BT-A in the right footpad of rats in the carrageenan-induced inflammation model. Furthermore, the group in which the antitoxin was administered showed a statistically reduced amount of the cleaved SNAP-25 protein, which suggests the possibility of the transsynaptic transfer of BT-A at the level of the spinal cord. These observations invite further research into the transsynaptic transfer mechanism of BT-A.