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成年大鼠颈上神经节中M胆碱能受体结合及氧化酶活性:6-羟基多巴胺和神经生长因子的作用

Muscarinic receptor binding and oxidative enzyme activities in the adult rat superior cervical ganglion: effects of 6-hydroxydopamine and nerve growth factor.

作者信息

Dombrowski A M, Jerkins A A, Kauffman F C

出版信息

J Neurosci. 1983 Oct;3(10):1963-70. doi: 10.1523/JNEUROSCI.03-10-01963.1983.

Abstract

Administration of 6-hydroxydopamine to adult rats results in changes in the superior cervical ganglion similar to those noted after axotomy; namely, a decrease in muscarinic receptor binding and increases in activities of the oxidative enzymes of the pentose phosphate pathway. These changes were either prevented or attenuated markedly by the systemic administration of nerve growth factor. Administration of nerve growth factor alone did not significantly increase N-methylscopolamine binding in the ganglion or reduce the activities of the oxidative enzymes. Explants of the ganglion maintained in serum-free medium over a period of 3 days demonstrated increases in oxidative enzyme activity and a decrease in N-methylscopolamine binding. Addition of 20 nM nerve growth factor to the culture medium prevented the decline in N-methylscopolamine binding in ganglion explants. The increases in oxidative enzyme activities were unaltered. Addition of high amounts of nerve growth factor, 200 nM, resulted in a significant increase in tyrosine hydroxylase activity but no further increase in N-methylscopolamine binding in ganglion explants. Glucocorticoids added to the culture medium did not affect the muscarinic binding or enzyme activities. Thus, decreases in muscarinic binding activity which occur in the superior cervical ganglion after axotomy or 6-hydroxydopamine treatment may be explained by a loss of nerve growth factor supplied to the ganglion. Increases in the oxidative enzymes of the pentose phosphate pathway that occur in the ganglion after axonal injury appear to involve additional factors.

摘要

给成年大鼠注射6-羟基多巴胺会导致颈上神经节发生变化,类似于轴突切断后所观察到的变化;即毒蕈碱受体结合减少,磷酸戊糖途径氧化酶活性增加。全身给予神经生长因子可显著预防或减轻这些变化。单独给予神经生长因子不会显著增加神经节中N-甲基东莨菪碱的结合,也不会降低氧化酶的活性。在无血清培养基中培养3天的神经节外植体显示氧化酶活性增加,N-甲基东莨菪碱结合减少。向培养基中添加20 nM神经生长因子可防止神经节外植体中N-甲基东莨菪碱结合的下降。氧化酶活性的增加未改变。添加大量神经生长因子(200 nM)可导致酪氨酸羟化酶活性显著增加,但神经节外植体中N-甲基东莨菪碱的结合没有进一步增加。添加到培养基中的糖皮质激素不影响毒蕈碱结合或酶活性。因此,轴突切断或6-羟基多巴胺处理后颈上神经节中发生的毒蕈碱结合活性降低可能是由于供应给神经节的神经生长因子丧失所致。轴突损伤后神经节中磷酸戊糖途径氧化酶的增加似乎涉及其他因素。

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