One ion channel that models the thermal hyperalgesia induced by proinflammatory factors is the integrator of pain ion channel TRPV1 (transient receptor potential vanilla type I). The TRPV1 is a calcium-permeable channel which can be activated by capsaicin, acid pH extracellular and temperatures above 43 º C, which is located on the peripheral terminals of nociceptors, where the detector harmful levels of heat.

The contribution of TRPV1 to heat hyperalgesia has been established both pharmacologically, through the evaluation of the effect of receptor antagonists, such as genetically generated a transgenic mouse (TRPV1-null). It was demonstrated that deletion of TRPV1 function significantly reduced the hypersensitivity to heat in inflammatory conditions and also that the ion channel activity was increased by proinflammatory mediators. The group of Ferrer-Montiel, Institute of Molecular and Cell Biology, University Miguel Hernández (Alicante), has investigated the involvement of regulated exocytosis in TRPV1 sensitization caused by inflammatory agents proalgésicos in certain rat sensory neurons.

In particular, we have studied the contribution of SNARE complex-dependent exocytosis (N-ethylmaleimide-sensitive factor attachment protein receptor) using a small peptide derived from the sequence of the protein SNAP-25, which acts as a potent specific inhibitor neuronal exocytosis. It seems that in this animal model, some pro-inflammatory agents, but not all, sensitize nociceptors to promote the recruitment of channels TRVP1 the neuronal surface. This supports the principle that the exocytosis of TRPV1-mediated SNARE complex may be a therapeutic target for treating inflammatory pain.