Botulinum toxin type A (BT-A) is a potent neurotoxin produced by the bacterium Clostridium botulinum. Its mechanism of action is based on preventing the release of neurotransmitters into the synaptic cleft by proteolytically cleaving SNARE proteins responsible for their exocytosis. For a long time, it was believed that the effects of BT-A were limited to the peripheral areas where it was applied, restricting its therapeutic use to treating autonomic disorders, localized spasticity, and hyperkinetic movement disorders. Over time, it was established that BT-A has significant antinociceptive effects at the central level, with minimal side effects, long-lasting impact, and no development of tolerance compared to other systemically acting analgesics, making it an exceptionally attractive candidate for further research, particularly in the treatment of chronic pain. The aim of this thesis was to investigate the influence of BT-A on the expression of CGRP, a neuropeptide mediator of pain and inflammation, in the trigeminal ganglion in a model of inflammatory orofacial pain induced by formalin application in rats. BT-A (7 i.j./kg) was unilaterally administered to the area of the right facial vibrissae (ipsilateral) in Wistar rats. Six days later, pain was induced in the area of the left facial vibrissae (contralateral) by applying 50 μL of 2.5% formalin, after which the animals were sacrificed and sections of their trigeminal ganglia were analyzed. In the negative control group, saline was used instead of BT-A, administered bilaterally, while in the positive control group, saline was administered ipsilaterally, and 50 μL of 2.5% formalin was applied contralaterally. Immunohistochemical analysis and statistical processing were used to monitor and quantify the intensity of CGRP signals in transverse sections of the trigeminal ganglia. In the experimental group, a statistically significant reduction in CGRP expression was observed compared to the control group. The obtained results suggest that BT-A also acts on the opposite side of the application site, indicating its potential for axonal transport and possible trans-synaptic transfer (transcytosis). In conclusion, this thesis demonstrates that BT-A can act not only at the local level but also at the central nervous system level through potential transcytosis, opening up the possibility for further research into its central antinociceptive effects.