Miettinen R, Kotti T, Halonen T, Riekkinen P
Department of Neurology, University of Kuopio, Finland.
Eur J Neurosci. 1995 Aug 1;7(8):1822-5. doi: 10.1111/j.1460-9568.1995.tb00701.x.
Neurons containing nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase exhibit high resistance to several excitotoxins. In the neocortex and striatum, however, these neurons are sensitive to kainic acid. Here we report that, 2 weeks after i.p. injection of kainic acid, the number of NADPH diaphorase neurons in the hilus and CA1 subfield was decreased, whereas the cell counts in the other hippocampal areas were to a great extent similar to those for the controls. We propose that the loss of NADPH diaphorase neurons in the hippocampus after systemic injection of kainic acid is associated with the pathophysiological processes involved in the spreading of epileptic seizure activity rather than to the direct neurotoxic effect of the kainic acid per se.
含有烟酰胺腺嘌呤二核苷酸磷酸（NADPH）黄递酶的神经元对几种兴奋性毒素具有高度抗性。然而，在新皮层和纹状体中，这些神经元对海人酸敏感。在此我们报告，腹腔注射海人酸2周后，海马门和CA1亚区中NADPH黄递酶神经元的数量减少，而其他海马区域的细胞计数在很大程度上与对照组相似。我们提出，全身注射海人酸后海马中NADPH黄递酶神经元的丧失与癫痫发作活动扩散所涉及的病理生理过程有关，而非与海人酸本身的直接神经毒性作用有关。
