Previous studies suggested that polymodal capsaicin-sensitive TRPV1 ion channel could also be a receptor for nitric oxide (NO). However, the evidence for this notion is based on rather indirect experiments, which questions its physiological relevance. The present paper provides an improved method of application of NO donors such as sodium nitroprusside (SNP) in an electrophysiological experiment, implying the simultaneous delivery of sulfhydryl-containing reagents such as L-cysteine (L-Cys) that facilitates the release of NO from a donor substance and allows inducing macroscopic TRPV1- mediated current. We found that external application of 100 μM SNP per se onto dorsal root ganglia (DRG) neurons responsive to capsaicin cannot activate TRPV1 ion channel. In contrast, the application of SNP simultaneously with 100 μM L-Cys induces transmembrane current with features characteristic of TRPV1-mediated one, i.e., inward at command membrane potential (Vcomm) +50 mV, outward at Vcomm -100 mV, and susceptible to blockade with capsazepine, a selective TRPV1 antagonist. At the same time, the application of L-Cys itself evoked no response in conditions tested. To summarize, our work confirms the assumption about the sensitivity of TRPV1 to NO and provides a simple method for further studies of their interaction.