**1. Introduction**

Pain is an essential sense that has evolved in complex organisms to minimize cell and tissue damage and thus increase survival. The onset of pain results in the adoption of behaviors that apart the body from a "dangerous environment" and allow tissue repair. Pain also protects us from our environment, by teaching us what situations and behaviors are likely to lead to injury. Pain pathways operate at numerous levels in the nervous system and are under voluntary and involuntary control. The neural process through which organisms encode noxious stimuli is called nociception, and is mediated by the activation of sensory terminals called nociceptors. Blocking these processes with analgesics has been a major pharmaceutical achievement [1].

Humans have nine subtypes of voltage-gated sodium channels (Nav), denoted from Nav 1.1 to Nav 1.9 and which are expressed in various organs; Nav 1.1, Nav 1.2, Nav 1.3 and Nav 1.6 channels predominate in the central nervous system, while Nav1.7, Nav 1.8 and Nav 1.9 are mainly expressed in the peripheral nervous system, Nav 1.4 channels are expressed in skeletal muscle and Nav 1.5 in the heart. Of all of them, the Nav1.7, Nav 1.8 and Nav 1.9 channels play an important role in pain signaling [2, 3].

The Nav1.7 channel has been shown to play a crucial role in pain sensation and there is interesting genetic evidence linking Nav1.7 and the gene encoding it SCN9A to pain disorders in humans [4].
