Perrone M H, Lepore R D, Shain W
J Pharmacol Exp Ther. 1986 Aug;238(2):389-95.
Substance P (SP) receptors were described by the specific binding of [3H]SP to several neuronal and glial cell lines. The neuronal cell lines N18 and NG108-15 were found to contain few if any SP receptors (less than 5 fmol/mg of protein). The glial cell line LRM55 contained large numbers (Bmax = 707 fmol/mg of protein) of a single class of SP binding sites (Kd = 276 pM). [3H]SP binding could be inhibited by a number of c-terminal SP fragments and the tachykinins physalaemin, eledoisin and kassinin. The binding kinetics and pharmacology of these receptors are similar to those the authors have previously described in the brain. Activation of SP receptors was shown to inhibit cyclic AMP-dependent, beta adrenergic-stimulated taurine release from LRM55 glial cells. SP inhibition must occur by mechanisms affecting taurine release after adenylate cyclase activation, inasmuch as SP has no significant effect on beta adrenergic-stimulated increases or basal levels of intracellular cyclic AMP.
P物质（SP）受体是通过[³H]SP与几种神经元和神经胶质细胞系的特异性结合来描述的。发现神经元细胞系N18和NG108 - 15即使含有SP受体也很少（每毫克蛋白质少于5飞摩尔）。神经胶质细胞系LRM55含有大量（Bmax = 707飞摩尔/毫克蛋白质）单一类型的SP结合位点（Kd = 276皮摩尔）。[³H]SP结合可被多种C末端SP片段以及速激肽 Physalaemin、Eledoisin和Kassinin抑制。这些受体的结合动力学和药理学与作者先前在大脑中描述的相似。SP受体的激活被证明可抑制LRM55神经胶质细胞中依赖环磷酸腺苷（cAMP）的β肾上腺素能刺激的牛磺酸释放。由于SP对β肾上腺素能刺激的细胞内cAMP增加或基础水平没有显著影响，因此SP抑制必定是通过影响腺苷酸环化酶激活后牛磺酸释放的机制发生的。
