Thermal properties of acid-induced depolarization in cultured rat small primary afferent neurons.

Tissue ischemia and inflammation result in localized acidosis, and acidic pH can trigger a sensation of pain. Pain is known to be often modified by the tissue temperature. The purpose of this study is to clarify the thermal behavior of nociceptors in response to acidification using intracellular recordings from cultured rat primary afferent neurons. Extracellular acidification induced depolarization of two types, transient and sustained responses. The former (to pH 6.3 and 5.2) was augmented at lower temperature (26, 16 degrees C) and amiloride blocked the response to pH 6.3 at 26 degrees C. On the other hand, the sustained depolarization, which often followed the transient one, in response to pH 6.3 was greater at 36 degrees C and significantly blocked by capsazepine at 36 degrees C, but not at 26 degrees C. The sustained response to pH 5.2 was blocked even at 26 degrees C. These results suggest that the low pH evoked depolarization is temperature-dependent, and the contribution of transient receptor potential V1 (vanilloid receptor 1) to proton-induced response is greater in the physiological body temperature range, while that of the acid-sensing-ion-channel family is greater at room temperature or lower.