Concluding Remarks

Molecular mechanisms of the nociceptive information control in primary sensory neuron are described based on our investigation of the membrane signaling cascade (opioid-like receptor → Na+,K+-ATPase → NaV1.8 channel). Summarizing the data presented in this volume it is possible to conclude that modulation of NaV1.8 channels responsible for the coding of noxious signals can be carried out due to two novel targeting mechanisms. The first of these is the activation of opioid-like receptors; the second is the activation of the Na+,K+-ATPase signal-transducing function. Development of a novel class of analgesics that trigger these mechanisms should lead in the near future to successful solution of the problem of chronic pain relief.

Keywords: Analgesic, Modulated receptor, NaV1.8 channels, Na+, K+-ATPase, nociception, Opioid-like receptor, Signal transducer.