Botulinum toxin type A (BTX-A) has been used to treat numerous clinical conditions characterised by muscle spasticity for years. Long-term antinociceptive effect of BTX-A after its single peripheal application has been reported in various experimental models of inflammatory and neuropathic pain. This, combined with its low side effects frequency differs BT-A from other currently used systemic painkillers. Until now, many preclinical and clinical studies have been conducted with the goal of discovering BT-A's exact mechanism and site of action in mind, which would allow for the expansion of current indications to many other pain conditions. In contrast to generally accepted theory of BTX-A's peripheral suppression of neurotransmitters release from sensory nerve endings, the results of several recent researches suggest its central site of action, most likely at the dorsal horn of spinal cord level, where peripherally applied BTX-A is delivered by retrograde axonal transport. There is also evidence that BTX-A has bilateral antinociceptive effect after its unilateral peripheral application. The goal of this master's thesis was to confirm these statements using inflammatory pain model where pain is inflicted by carrageenan injection into hindpaws of male Wistar rats. One group of animals was pretreated with a BTX-A dose of 7 i.u./kg, while another group was treated with BTX-A antitoxin (anti-BTX-A) alongside BTX-A. Control groups have received saline injection (0,9 % NaCl) instead of BTX-A and one of them was treated with saline instead of carrageenan in an attempt to avoid inflammation. Expression of c-Fos (neuronal activity marker), which was used as indirect pain indicator, was imunohistochemically examined in L4/L5 cross sections of rat spinal cord. The results show that, in line with our expectations, carrageenan is enabling bilateral activation of spinal neurons while BTX-A reduced this activation on both sides of the spinal cord. Statistically significant reduction of c-Fos expression was recorded in comparison with control group and with experimental group treated with anti-BTX-A on both the ipsilateral and contralateral side of spinal cord. This is just another proof that BTX-A is exerting its antinociceptive effects centrally, with both sides of spinal cord as its site of action.