Self-inhibition in Ca2+ -evoked taste responses: a novel tool for functional dissection of salt taste transduction mechanisms.
Self-inhibition in Ca2+ -evoked taste responses: a novel tool for functional dissection of salt taste transduction mechanisms.
复制标题
Ca2 诱发味觉反应的自我抑制：盐味转导机制功能剖析的新工具。
DOI：
10.1152/jn.1998.79.2.911
复制
发表时间：
1998
影响因子：
2.5
通讯作者：
DeSimone,JA
中科院分区：
文献类型：
--
作者：
Kloub,MA;Heck,GL;DeSimone,JA
Kloub, Mamoun A, Gerard L. Heck和John A. DeSimone。钙离子诱导味觉受体的自我抑制：盐味转导机制功能解剖的新工具。中国生物医学工程学报。32(2):387 - 398。在舌感受野同时夹持电流和电压的情况下，获得了大鼠鼓室索（CT）对cacl2的反应。与大多数其他盐不同，cacl2诱导负向上皮电位，并在超过临界浓度时产生自我抑制的CT反应。CT反应以剂量依赖的方式增加到~ 0.3 M，之后随着浓度的增加而降低。在Ca2+自抑的浓度下，它也抑制了对NaCl、KCl和NH4Cl的反应，这些反应存在于CaCl2的混合物中。Ca2+完全阻断了NaCl CT响应的酰胺不敏感部分、整个kcl诱发的CT响应以及NH4Cl（≥0.3 M）的高浓度域CT响应。三种Cl -盐（Na+， K+和NH+4）的响应之间重叠的Ca2+敏感性表明一个共同的，Ca2+敏感的转导途径。细胞外Ca2+已被证明通过降低紧密连接的水渗透性和阳离子电导来调节不同上皮细胞系的细胞旁通路。Ca2+诱导的紧密连接的调制与Ca2+结合到固定的负位点有关。这导致离子选择性从阳离子到阴离子的转换，我们也通过在CT记录期间同时监测上皮电位在我们的系统中观察到。这些数据表明，细胞旁通路是CaCl2taste反应的刺激和调节位点。此外，它们表明NaCl、KCl和NH4Cl味觉接收的重要转导位点只能通过细胞旁通路到达。更普遍的是，他们表明Ca2+在完整上皮中对细胞旁运输的调节在系统水平上具有功能后果。
Kloub, Mamoun A., Gerard L. Heck, and John A. DeSimone.Self-inhibition in Ca2+-evoked taste receptors: a novel tool for functional dissection of salt taste transduction mechanisms.J. Neurophysiol.79: 911–921, 1998. Rat chorda tympani (CT) responses to CaCl2were obtained during simultaneous current and voltage clamping of the lingual receptive field. Unlike most other salts, CaCl2induced negatively directed transepithelial potentials and gave CT responses that were auto-inhibitory beyond a critical concentration. CT responses increased in a dose-dependent manner to ∼0.3 M, whereafter they decreased with increasing concentration. At concentrations where Ca2+was self-inhibitory, it also inhibited responses to NaCl, KCl, and NH4Cl present in mixtures with CaCl2. Ca2+completely blocked the amiloride-insensitive component of the NaCl CT response, the entire KCl-evoked CT response, and the high-concentration-domain CT responses of NH4Cl (≥0.3 M). The overlapping Ca2+-sensitivity between the responses of the three Cl−salts (Na+, K+, and NH+4) suggests a common, Ca2+-sensitive, transduction pathway. Extracellular Ca2+has been shown to modulate the paracellular pathways in different epithelial cell lines by decreasing the water permeability and cation conductance of tight junctions. Ca2+-induced modulation of tight junctions is associated with Ca2+binding to fixed negative sites. This results in a conversion of ion selectivity from cationic to anionic, which we also observed in our system through simultaneous monitoring of the transepithelial potential during CT recording. The data indicate the paracellular pathway as the stimulatory and modulatory site of CaCl2taste responses. In addition, they indicate that important transduction sites for NaCl, KCl, and NH4Cl taste reception are accessible only through the paracellular pathways. More generally, they show that modulation of paracellular transport by Ca2+in an intact epithelium has functional consequences at a systemic level.