Reubi J C, Palacios J M, Maurer R
Neuroscience. 1987 Jun;21(3):847-56. doi: 10.1016/0306-4522(87)90041-8.
Using the iodinated luteinizing-hormone-releasing hormone analogue [D-Ala6, N alpha MeLeu7, Pro9 NEt]-luteinizing-hormone-releasing hormone as radioligand, specific binding sites have been visualized in the rat both in the pituitary and the hippocampal formation of the brain. In the hippocampus, the CA1, CA2 and particularly CA3 regions were heavily labelled. These hippocampal sites have a pharmacological specificity resembling that of luteinizing-hormone-releasing hormone receptors in pituitary homogenates and could therefore represent true luteinizing-hormone-releasing hormone receptors. The luteinizing-hormone-releasing hormone superagonist [D-Ala6, Pro9 NEt]-luteinizing-hormone-releasing hormone and the potent antagonist [D-pGlu1, D-Phe2, D-Trp3,6]-luteinizing-hormone-releasing hormone were highly potent in displacing the iodinated luteinizing-hormone-releasing hormone analogue. The weak agonist [Gln8]-luteinizing-hormone-releasing hormone, however, was at least two orders of magnitude less potent. Somatostatin was inactive. Hippocampal luteinizing-hormone-releasing hormone receptors were species-specific, being present in the rat but not in the mouse, guinea-pig, hamster, rabbit and human brains. In order to identify the cellular location of these hippocampal receptors, various lesions were performed. Electrolytic lesions of the septal afferents did not reveal any receptor density change. Colchicine as well as kainic acid injections did, however, reduce considerably the number of hippocampal receptors. Interestingly, in the electrolytically and kainic-acid-lesioned animals, the appearance of non-displaceable luteinizing-hormone-releasing hormone binding sites within a well-defined area corresponding to the lesioned, gliosis-rich area was observed. The present results suggest the presence of pharmacologically specific, species-dependent, luteinizing-hormone-releasing hormone receptors located, at least partly, on intrinsic hippocampal neurons, in particular granule and pyramidal cells.
以碘化促黄体生成激素释放激素类似物[D - Ala6, NαMeLeu7, Pro9 NEt] - 促黄体生成激素释放激素作为放射性配体，在大鼠的垂体和脑的海马结构中均已观察到特异性结合位点。在海马体中，CA1、CA2区域，尤其是CA3区域标记明显。这些海马体位点具有与垂体匀浆中促黄体生成激素释放激素受体相似的药理学特异性，因此可能代表真正的促黄体生成激素释放激素受体。促黄体生成激素释放激素超级激动剂[D - Ala6, Pro9 NEt] - 促黄体生成激素释放激素和强效拮抗剂[D - pGlu1, D - Phe2, D - Trp3,6] - 促黄体生成激素释放激素在置换碘化促黄体生成激素释放激素类似物方面具有高效能。然而，弱激动剂[Gln8] - 促黄体生成激素释放激素的效能至少低两个数量级。生长抑素无活性。海马体促黄体生成激素释放激素受体具有物种特异性，存在于大鼠脑中，但不存在于小鼠、豚鼠、仓鼠、兔和人脑中。为了确定这些海马体受体的细胞定位，进行了各种损伤实验。隔区传入纤维的电解损伤未显示受体密度有任何变化。然而，注射秋水仙碱和 kainic 酸确实显著减少了海马体受体的数量。有趣的是，在电解损伤和 kainic 酸损伤的动物中，在对应于损伤的、富含胶质细胞增生区域的一个明确区域内观察到了不可置换的促黄体生成激素释放激素结合位点的出现。目前的结果表明存在药理学特异性、物种依赖性的促黄体生成激素释放激素受体，这些受体至少部分位于海马体固有神经元上，特别是颗粒细胞和锥体细胞。
