Dragunow M, Goulding M, Faull R L, Ralph R, Mee E, Frith R
Department of Anatomy, School of Medicine, University of Auckland, New Zealand.
Exp Neurol. 1990 Mar;107(3):236-48. doi: 10.1016/0014-4886(90)90141-e.
Focal brain injury in mice induced c-fos mRNA and protein in neurons throughout the damaged neocortex, including the piriform and the entorhinal cortices, as well as in nonneural brain cells (e.g., glia, pia, ependyma). The pattern of c-fos induction after injury suggested that injury led to spreading depression which then led to c-fos induction in neurons. Human neurons in the temporal cortex and hippocampus also showed c-fos protein induction after neurosurgical trauma. The c-fos mRNA and protein induction in mouse neurons was prevented by the noncompetitive NMDA antagonist ketamine but only partially inhibited by the voltage-dependent calcium channel antagonist nifedipine and the calmodulin antagonist trifluoperazine. The c-fos protein induction in nonneural brain cells after injury was not affected by these drugs. Thus, induction of c-fos in neocortical neurons after focal brain injury is partly NMDA receptor mediated.
小鼠局灶性脑损伤可诱导受损新皮质（包括梨状皮质和内嗅皮质）以及非神经脑细胞（如神经胶质细胞、软脑膜、室管膜）中的神经元产生c-fos mRNA和蛋白质。损伤后c-fos的诱导模式表明，损伤导致了扩散性抑制，进而导致神经元中c-fos的诱导。神经外科创伤后，颞叶皮质和海马体中的人类神经元也显示出c-fos蛋白的诱导。非竞争性NMDA拮抗剂氯胺酮可阻止小鼠神经元中c-fos mRNA和蛋白质的诱导，但电压依赖性钙通道拮抗剂硝苯地平和钙调蛋白拮抗剂三氟拉嗪只能部分抑制这种诱导。损伤后非神经脑细胞中c-fos蛋白的诱导不受这些药物的影响。因此，局灶性脑损伤后新皮质神经元中c-fos的诱导部分由NMDA受体介导。
