Oral Sensory mechanism of Capsaicin and thermal stimulation

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The ingestion of spicy food containing hot chili peppers evokes an oral tingling and burning sensation. Much interest in pain perception has recently focused on capsaicin, the pungent ingredient in hot pepper, and its molecular target, vanilloid receptor 1 (TRPV1, VR1), which is a nociceptive-specific cation channel. We demonstrated that the taste papillae of the tongue and palate are richly innervated with TRPV1 immunoreactive nerves. It is well known that extracellular signal-regulated kinase (ERK) is a mitogen activated protein kinase (MAPK) that mediates several cellular responses to mitogenic and differentiation signals. MAPK are activated not only during growth factor signaling but in neuronal plasticity as well. Very recently it is reported that phosphorylation of ERK in primary afferent neurons occurred in response to noxious stimulation of the peripheral nerve. Then, to elucidate the sensory mechanisms of oral sensation, including hot taste, we examined the rapid phosphorylation of ERK (pERK) in primary afferent nerves in the oral mucosa after stimulation with capsaicin to the oral cavity. After intraoral capsaicin stimulation, the amount of pERK labeling was clearly increased compared with the vehicle treated rats. Interestingly, abundant labeled fibers were observed in the taste buds of circumvallate and foliate papillae. The pERK-labeled nerves were also labeled with P2X3 or CGRP. Some of the nerves were labeled with IB4 lectin. Capsaicin stimulation caused rapid phosphorylation of ERK in the peripheral nerves of the oral mucosa, suggesting that these nerves are of great importance in the perception of capsaicin and that ERK activation is involved in oral sensitization.