Szerb J C, Hadházy P, Dudar J D
Brain Res. 1977 Jun 10;128(2):285-91. doi: 10.1016/0006-8993(77)90995-7.
To establish the existence and sensitivity of presynaptic muscarinic receptors on central cholinergic neurons, the electrically evoked release of [3H]ACh from hippocampal slices was measured after medial septal lesion or in the presence of graded concentrations of muscarinic agonists and antagonists. One week after septal lesion, the evoked release of [3H]ACh was abolished, indicating that septo-hippocampal cholinergic fibres are the source of this release. The muscarinic agonists, Oxotremorine, carbamylcholine and arecoline reduced the rate of evoked release of [3H]ACh with an ED50 similar to the ED50 required to displace specific [3H]quinuclidinyl benzilate (QNB) binding as found by Yamamura and Snyder. However, the antagonists QNB, antropine and scopolamine were 10 times weaker in increasing the rate of [3H]ACh release than in displacing [3H]QNB binding. Results suggest that the lower affinity of muscarinic antagonists to presynaptic receptors prevents the demonstration of the specific labelling of these receptors with [3H]QNB.
为了确定中枢胆碱能神经元上突触前毒蕈碱受体的存在及其敏感性，在内侧隔区损伤后或在存在不同浓度的毒蕈碱激动剂和拮抗剂的情况下，测量了海马切片中电诱发的[3H]乙酰胆碱（ACh）释放。隔区损伤一周后，诱发的[3H]ACh释放被消除，这表明隔区 - 海马胆碱能纤维是这种释放的来源。毒蕈碱激动剂氧化震颤素、氨甲酰胆碱和槟榔碱降低了诱发的[3H]ACh释放速率，其半数有效剂量（ED50）与Yamamura和Snyder发现的置换特异性[3H]喹核醇基苯甲酸酯（QNB）结合所需的ED50相似。然而，拮抗剂QNB、阿托品和东莨菪碱在增加[3H]ACh释放速率方面的作用比置换[3H]QNB结合的作用弱10倍。结果表明，毒蕈碱拮抗剂对突触前受体的亲和力较低，妨碍了用[3H]QNB对这些受体进行特异性标记的显示。
