Nagata N, Harada N, Chen L, Cho H, Tomoda K, Yamashita T
Department of Otolaryngology, Kansai Medical University, Osaka, Japan.
Acta Otolaryngol. 2000 Sep;120(6):704-9. doi: 10.1080/000164800750000216.
Extracellular adenosine 5'-triphosphate (ATP)-induced intracellular calcium concentration ([Ca2+]i) changes in acutely isolated vestibular ganglion cells (VGCs) of the guinea pig were investigated using the Ca2+ -sensitive dye Fura-2. Extracellular ATP induced an increase in [Ca2+]i in VGCs in a dose-dependent manner. ATP induced an increase in [Ca2+]i even in the absence of extracellular Ca2+ (1 mM Ethylene Glycol-bis (beta-aminoethyl Ether) N,N,N',N'-Tetraacetic Acid (EGTA)), thus suggesting that ATP induces Ca2+ release from the intracellular stores. The P2-receptor antagonists suramin and reactive blue 2 inhibited the ATP-induced [Ca2+]i increase in a dose-dependent manner. The P1-receptor agonist adenosine did not induce any changes in [Ca2+]i. These results suggest that VGCs may possess a P2-purinergic receptor but not a P1-purinergic receptor. La3+, a receptor-mediated calcium channel blocker, inhibited the ATP-induced [Ca2+]i increase but, in contrast, nifedipine, a L-type calcium channel blocker, did not. These results suggest that ATP induces both a Ca2+ -release from the intracellular stores and a Ca2+ influx from the extracellular space through La3+ -sensitive and nifedipine-insensitive Ca2+ channels in VGCs. Our results also suggest that extracellular ATP may act as a neurotransmitter or neuromodulator of the vestibular peripheral system in the guinea pig.
使用钙敏染料Fura-2研究了细胞外5'-三磷酸腺苷(ATP)诱导的豚鼠急性分离前庭神经节细胞(VGCs)内钙浓度([Ca2+]i)的变化。细胞外ATP以剂量依赖性方式诱导VGCs中[Ca2+]i升高。即使在没有细胞外钙(1 mM乙二醇双(β-氨基乙基醚)N,N,N',N'-四乙酸(EGTA))的情况下,ATP也能诱导[Ca2+]i升高,这表明ATP诱导细胞内钙库释放钙。P2受体拮抗剂苏拉明和活性蓝2以剂量依赖性方式抑制ATP诱导的[Ca2+]i升高。P1受体激动剂腺苷未诱导[Ca2+]i发生任何变化。这些结果表明,VGCs可能具有P2嘌呤能受体,但不具有P1嘌呤能受体。受体介导的钙通道阻滞剂La3+抑制ATP诱导的[Ca2+]i升高,但相反,L型钙通道阻滞剂硝苯地平则没有。这些结果表明,ATP在VGCs中既诱导细胞内钙库释放钙,又通过对La3+敏感而对硝苯地平不敏感的钙通道诱导细胞外钙内流。我们的结果还表明,细胞外ATP可能作为豚鼠前庭外周系统的神经递质或神经调节剂发挥作用。