Change in excitability and phenotype of substance P and its receptor in cat Aβ sensory neurons following peripheral inflammation

Abstract

The effect of peripheral inflammation on spontaneous firing and level of substance P (SP) and its receptor in electrophysiologically identified cat Aβ neurons of dorsal root ganglion (DRG) was studied in vivo using a combination of intracellular recording, dye injection and immunohistochemical techniques. Following injection of carrageenan (Carg) into cat hindpaw, the number of Aβ neurons with spontaneous firing was enhanced significantly (42.9%, n=182) in comparison with control (16.8%, n=149, P<0.01). DRG Aβ neurons became less depolarized 2–4 h following Carg injection. After identifying the cell properties, Lucifer Yellow was injected and SP-like immunoreactivity (SP-LI) was then detected. A total of 17% of Aβ sensory neurons exhibited SP-LI in inflammatory cat. We also found in rat DRGs that the number of SP-LI positive large cells (>35 μm) was also significantly increased in Carg-treated DRG (11.8±1.2, n=8) compared with untreated DRG (1.8±0.8, n=8, P<0.01). In control cat, the topical use of SP in DRG did not induce any response of Aβ neurons. However, in Carg-treated cat, SP depolarized the membrane potential in most Aβ neurons (68.2%, n=22). L668,169, an antagonist of SP receptor, completely blocked the SP-induced responses. Furthermore, repeated application of SP did not induce obvious desensitization of Aβ neurons. These data suggest that peripheral inflammation increased the excitability, SP level and sensitivity of SP receptor of Aβ neurons. Therefore, we concluded that Aβ sensory neurons appear to contribute to inflammatory allodynia.