Jonakait G M, Wei R, Sheng Z L, Hart R P, Ni L
Department of Biological Sciences, Rutgers University, Newark, New Jersey 07102.
Neuron. 1994 May;12(5):1149-59. doi: 10.1016/0896-6273(94)90322-0.
In cultured rat embryonic septal nuclei with adjacent basal forebrain, murine interferon-gamma (IFN gamma) produces a striking increase in choline acetyltransferase (ChAT) activity and mRNA. The effect of IFN gamma on cholinergic differentiation is more potent in E14 cultures than in older cultures. IFN gamma does not cause a change in the affinity of ChAT for choline, nor does it affect cell proliferation. Whereas IFN gamma doubles neuronal cell number, the cholinergic cell number increases more than 7-fold. Ameboid microglia respond to IFN gamma with the translocation of p91 to the nucleus. The action of IFN gamma is not mediated by NGF or bFGF. The enhancement of cholinergic expression that occurs with increased cell density may be partly attributable to an endogenous IFN gamma-like molecule, since antibodies to IFN gamma offset the effects of increased cell density.
在培养的大鼠胚胎隔核与相邻的基底前脑组织中，小鼠γ干扰素（IFNγ）可使胆碱乙酰转移酶（ChAT）的活性和mRNA显著增加。在胚胎第14天的培养物中，IFNγ对胆碱能分化的作用比在较老的培养物中更强。IFNγ不会导致ChAT对胆碱的亲和力发生变化，也不影响细胞增殖。虽然IFNγ可使神经元细胞数量增加一倍，但胆碱能细胞数量增加超过7倍。阿米巴样小胶质细胞对IFNγ的反应是p91转位至细胞核。IFNγ的作用不是由神经生长因子（NGF）或碱性成纤维细胞生长因子（bFGF）介导的。随着细胞密度增加而出现的胆碱能表达增强可能部分归因于一种内源性IFNγ样分子，因为针对IFNγ的抗体可抵消细胞密度增加的影响。
