Haddad G G, Jiang C
Department of Pediatrics, Yale University, School of Medicine, New Haven, Conn. 06520.
Biol Neonate. 1994;65(3-4):160-5. doi: 10.1159/000244046.
There has been an explosion in our understanding of how nerve cells in mammals respond to O2 deprivation and what are the mechanisms involved in nerve cell injury or survival. This is due to the development of new approaches, techniques and the clinical importance of brain ischemia and hypoxia. Recently, we have focussed on some issues pertaining to brain hypoxia in the newborn and adult. We have demonstrated that during anoxia intracellular K+ decreases significantly in nerve cells and that this K+ efflux is mediated by K+ channels that are sensitive to ATP. We have preliminary evidence that the activation of these channels attenuates the anoxia-induced depolarization in medullary neurons and can play a role in cell survival during anoxia. Further, we have characterized the distribution of these receptors/channels complexes in the CNS of the rat and in an anoxia-resistant animal: the turtle. These channels are present mainly in the cortex, substantia nigra and the cerebellum. Whole cell recordings (dissociated cells) established that these channels are postsynaptic in nature in medullary neurons. Single-channel recordings from our laboratory and those of others have started to reveal the intricacies of the regulation of these channels in excitable cells in general and in nerve cells in particular.
我们对哺乳动物神经细胞如何应对缺氧以及神经细胞损伤或存活所涉及的机制的理解有了飞跃式发展。这得益于新方法、新技术的发展以及脑缺血和缺氧的临床重要性。最近，我们专注于新生儿和成人脑缺氧的一些相关问题。我们已经证明，在缺氧期间，神经细胞内的钾离子（K⁺）显著减少，并且这种钾离子外流是由对三磷酸腺苷（ATP）敏感的钾离子通道介导的。我们有初步证据表明，这些通道的激活可减弱缺氧诱导的延髓神经元去极化，并在缺氧期间的细胞存活中发挥作用。此外，我们已经确定了这些受体/通道复合物在大鼠中枢神经系统以及抗缺氧动物——乌龟中的分布。这些通道主要存在于大脑皮层、黑质和小脑中。全细胞记录（分离细胞）表明，这些通道在延髓神经元中本质上是突触后通道。我们实验室以及其他实验室的单通道记录已开始揭示这些通道在一般可兴奋细胞，尤其是神经细胞中的调节复杂性。
