Fisher S K, Frey K A, Agranoff B W
J Neurosci. 1981 Dec;1(12):1407-13. doi: 10.1523/JNEUROSCI.01-12-01407.1981.
The stimulation of phospholipid labeling by muscarinic agonists has been examined in nerve ending preparations from lesioned hippocampus in order to investigate the synaptic locus of the effect. Unilateral injections of the neurotoxin, ibotenic acid, into the hippocampus resulted in an extensive loss of nerve cells from both the dentate gyrus and hippocampus on the lesioned side and a parallel loss of muscarinic receptors as revealed by [3H]quinuclidinyl benzilate autoradiography. Homogenates and nerve ending fractions prepared from the lesioned side of the hippocampus possessed a reduced specific activity (expressed per milligram of protein) of glutamic acid decarboxylase as well as a reduced number of muscarinic receptors compared with the control side. By contrast, choline acetyltransferase activity was either unchanged or slightly increased on the lesioned side. Although there was a reduced yield (25%) of nerve endings from the lesioned side, the specific activity of 32Pi incorporation into phospholipids in the absence of added carbachol was comparable to that of the control side. There was, however, a marked reduction in the carbachol stimulation of phosphatidic acid and phosphatidylinositol labeling in nerve ending fractions obtained from he lesioned hippocampus. These results indicate that the muscarinic receptors present in nerve ending fractions from hippocampus and implicated in stimulated phospholipid turnover are derived from cholinoceptive intrinsic neurons.
为了研究毒蕈碱激动剂对磷脂标记的刺激作用的突触位点，已在损伤海马的神经末梢制剂中对其进行了检测。向海马体单侧注射神经毒素鹅膏蕈氨酸，导致损伤侧齿状回和海马体的神经细胞大量丢失，同时通过[3H]喹核醇基苯甲酸酯放射自显影显示毒蕈碱受体也相应减少。与对照侧相比，从海马体损伤侧制备的匀浆和神经末梢部分的谷氨酸脱羧酶比活性（以每毫克蛋白质表示）降低，毒蕈碱受体数量也减少。相比之下，损伤侧的胆碱乙酰转移酶活性要么未改变，要么略有增加。尽管损伤侧神经末梢的产量降低了25%，但在不添加卡巴胆碱的情况下，32Pi掺入磷脂的比活性与对照侧相当。然而，从损伤海马体获得的神经末梢部分中，卡巴胆碱对磷脂酸和磷脂酰肌醇标记的刺激作用明显降低。这些结果表明，海马体神经末梢部分中存在的、与刺激磷脂周转有关的毒蕈碱受体源自胆碱能固有神经元。
