This study is aimed at understanding the mechanisms of nociceptive signaling in lamina X of the spinal cord, which are involved in the regulation of pain sensations. First, tetrodotoxin, which blocks action potentials, was applied to the system, which made it possible to isolate miniature synaptic activity (mEPSCs). After that, they added pidal, an agonist of TRPV1 receptors, which caused a significant increase in the frequency and amplitude of mEPSCs. Against the background of tetrodotoxin, the effect of capsaicin was biphasic: at first, the frequency of events increased sharply, after which it gradually decreased, but the amplitude increased. A control, without tetrodotoxin, application of capsaicin also caused an increase in synaptic activity, but this effect was not biphasic. Additional blockade of NMDA receptors (AP-5) partially reduced capsaicin-induced activity, while an AMPA receptor blocker (CNQX) almost completely abolished it, suggesting a critical role of glutamate receptors in maintaining this activity. The obtained results emphasize the importance of TRPV1 receptors in central sensitization and the possibility of its regulation, which opens new ways of modulation of chronic pain.