Complex pathophysiology of neuropathic pain involves various mechanisms on peripheral, spinal and supraspinal levels which are mediated by important neurotransmitters such as glutamate, GABA, glycine and transmembrane proteins like N-type calcium channels, TRPV1 vaniloid receptors and opioid μ-, δ- and κ-receptors. Numerous research has shown a significant role endogenous opioid system has in processes of transmission and modulation of pain. Experimental models of neuropathic pain show the enhacement of the activity of endogenous opioid system, and vast majority of envidence for the involment in the regulation of nociceptive processes on the spinal level has been found for enkephalins. However, in conditions like neuropathic pain, which is of chronic duration, the role of the opioid system can be notably altered. Analgetic effect of BT-A has been demonstrated in numerous preclinical and clinical studies in which BT-A significantly differs from other analgetics in terms that decreases pain for a long-term period (several months) after single local injection of small doses. In this work was measured enkephalin immunoreactivity by immunohistochemical methods in tissue samples of the dorsal horn of the spinal cord of three groups of animals; control animals, animals with neuropathic pain induced by partial transection of n. ishiadicus and animals with neuropathic pain which were injected with BT-A into the plantar surface of the hindpaw. We have shown bilateral increase in surface and intensity of immunoreactivity in group of animals which were injected with BT-A in comparison with control animals and animals with neuropathic pain. Taking everything into account, we can assume that BT-A indirectly increases the activty of endogenous opioid system by up-regulation of enkephalin synthesis. Further investigation which aim to correlate endogenous opioid system and antinociceptive effect of BT-A is needed in order to elucidate the central mechanism of action of BT-A and also in order to direct its clinical application as a new therapeutic option in treatment of neurophatic pain.