Jenison G L, Bobbin R P, Thalmann R
J Neurochem. 1985 Jun;44(6):1845-53. doi: 10.1111/j.1471-4159.1985.tb07178.x.
Guinea pig cochleae were perfused with high-potassium solutions to depolarize hair cells artificially and induce the release of afferent neurotransmitter. Sequential injections of artificial perilymph containing 5 mM KCl, then 50 mM KCl, and finally 5 mM KCl were made into the scala tympani. This injection sequence was conducted under either normal divalent-cation conditions (2.0 mM CaCl2, 1.0 mM MgCl2) or calcium-deficient conditions intended to antagonize evoked transmitter release (0.1 mM CaCl2, 20.0 mM MgCl2). The levels of 21 endogenous primary amines in effluent collected from the scala vestibuli were determined by gradient-elution, reverse-phase HPLC using o-phthaldialdehyde-thiol adducts with fluorescence detection. Analyses indicated effluent concentrations of glutamate, taurine, and a coeluting taurine-gamma-aminobutyrate (GABA) fraction (but not GABA alone) increased significantly after exposure to 50 mM KC1 and returned to baseline levels after reintroduction of 5 mM KC1 under normal divalent-cation conditions. Correspondent changes in the release of these constituents were significantly attenuated under calcium-deficient conditions. This was not the case for potassium-induced changes in the release of arginine, aspartate, and isoleucine. These data are consistent with the hypothesis that the receptoneuronal transmitter is glutamate and further suggest a calcium-dependent mechanism involving taurine.
用高钾溶液灌注豚鼠耳蜗，人为地使毛细胞去极化并诱导传入神经递质的释放。将含有5 mM氯化钾、然后50 mM氯化钾、最后5 mM氯化钾的人工外淋巴依次注入鼓阶。这种注射顺序是在正常二价阳离子条件（2.0 mM氯化钙、1.0 mM氯化镁）或旨在拮抗诱发递质释放的缺钙条件（0.1 mM氯化钙、20.0 mM氯化镁）下进行的。通过使用邻苯二甲醛-硫醇加合物的梯度洗脱、反相高效液相色谱法和荧光检测，测定从前庭阶收集的流出液中21种内源性伯胺的水平。分析表明，在正常二价阳离子条件下，暴露于50 mM氯化钾后，谷氨酸、牛磺酸和一种共洗脱的牛磺酸-γ-氨基丁酸（GABA）组分（但不是单独的GABA）的流出液浓度显著增加，重新引入5 mM氯化钾后恢复到基线水平。在缺钙条件下，这些成分释放的相应变化显著减弱。精氨酸、天冬氨酸和异亮氨酸释放的钾诱导变化则并非如此。这些数据与受体神经元递质是谷氨酸的假设一致，并进一步表明存在一种涉及牛磺酸的钙依赖机制。
