Abe K, Nakata A, Mizutani A, Saito H
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Neuropharmacology. 1994 Jul;33(7):847-52. doi: 10.1016/0028-3908(94)90180-5.
The role of the muscarinic cholinergic system in the generation of LTP in the medial perforant path-dentate granule cell synapses in vivo was investigated using anesthetized rats. Cholinergic denervation with AF64A, a cholinergic toxin, did not significantly affect LTP induced by a strong tetanus (100 pulses at 100 Hz), but attenuated the LTP induced by a weak tetanus (30 pulses at 60 Hz). The i.c.v. injection of scopolamine (1.5-50 nmol) did not significantly affect the LTP induced by the strong tetanus but attenuated the magnitude of LTP produced by the weak tetanus in a concentration-dependent manner. These results suggest that the cholinergic system is not essential for induction of LTP by strong stimuli but plays a role in facilitating the generation of LTP by weak stimuli. Furthermore, the induction of LTP by a weak tetanus was blocked by pirenzepine but affected by neither AF-DX116 nor 4-diphenylacetoxy-N-methylpiperidine. The LTP-facilitatory action of the cholinergic system is probably mediated by muscarinic M1 receptors.
利用麻醉大鼠研究了毒蕈碱胆碱能系统在体内内侧穿通通路-齿状颗粒细胞突触长时程增强（LTP）产生中的作用。用胆碱能毒素AF64A进行胆碱能去神经支配，对强强直刺激（100Hz，100个脉冲）诱导的LTP无显著影响，但减弱了弱强直刺激（60Hz，30个脉冲）诱导的LTP。脑室内注射东莨菪碱（1.5 - 50nmol）对强强直刺激诱导的LTP无显著影响，但以浓度依赖方式减弱了弱强直刺激产生的LTP幅度。这些结果表明，胆碱能系统对于强刺激诱导LTP并非必不可少，但在促进弱刺激产生LTP中发挥作用。此外，弱强直刺激诱导的LTP被哌仑西平阻断，但不受AF - DX116和4 - 二苯基乙酰氧基 - N - 甲基哌啶影响。胆碱能系统的LTP促进作用可能由毒蕈碱M1受体介导。
