Ueki A, Miyoshi K
Jpn J Psychiatry Neurol. 1987 Mar;41(1):87-96. doi: 10.1111/j.1440-1819.1987.tb00395.x.
Choline acetyltransferase (CAT) and glutamate decarboxylase (GAD) activities and [3H] quinuclidinyl benzilate ([3H]QNB) binding were determined in the rat frontal cortex following damage to the basal forebrain cholinergic system. Pre- and postsynaptic changes in the cholinergic system with the passage of time were also studied. After a unilateral injection of kainic acid into the right ventral globus pallidus, the GAD levels remained unaffected, but the CAT levels decreased to 63.4% after 7 days. After 12 weeks, the CAT levels had returned to 87% of the control value. The Bmax of [3H]QNB binding for the muscarinic receptor was higher in the ipsilateral cortex up to 4 weeks. On the other hand, the KD value at 12 weeks was higher without a change in the Bmax of the [3H]QNB binding. These findings might indicate an ongoing compensatory receptor mechanism of denervation supersensitivity as a response to early changes in presynaptic cholinergic activity and the production of postsynaptic effect with presynaptic cholinergic damage over a long period of time.
在大鼠基底前脑胆碱能系统受损后，测定其额叶皮质中的胆碱乙酰转移酶（CAT）和谷氨酸脱羧酶（GAD）活性以及[3H]喹核醇基苯甲酸酯（[3H]QNB）结合情况。同时还研究了胆碱能系统随时间推移的突触前和突触后变化。在右侧腹侧苍白球单侧注射海人酸后，GAD水平未受影响，但7天后CAT水平降至63.4%。12周后，CAT水平恢复至对照值的87%。在同侧皮质中，直至4周时，[3H]QNB与毒蕈碱受体结合的Bmax较高。另一方面，12周时的KD值较高，而[3H]QNB结合的Bmax没有变化。这些发现可能表明，作为对突触前胆碱能活性早期变化的一种反应，存在一种持续的去神经超敏反应的代偿性受体机制，并且在长时间内突触前胆碱能损伤会产生突触后效应。
