Lee K S, Tetzlaff W, Kreutzberg G W
Brain Res. 1986 Aug 13;380(1):155-8. doi: 10.1016/0006-8993(86)91440-x.
Adenosine A1 receptors, as demonstrated by [3H]cyclohexyladenosine (CHA) binding to cryostat sections of the brain, were studied utilizing quantitative autoradiographic techniques. A brief period of global CNS anoxia resulted in the rapid and persistent down regulation of [3H]CHA binding sites in the hippocampus but not in the neocortex or striatum. The density of adenosine A1 receptors in a given brain region has previously been shown to be a critical factor in determining the strength of the inhibitory action of adenosine. Since the down regulation of these sites is correlated temporally with the onset of hyperactivity following transient anoxia, it is suggested that a reduction in the strength of the neuromodulatory action of adenosine contributes to the postanoxic hyperactivity of CA1 pyramidal cells and perhaps to their selective vulnerability.
利用定量放射自显影技术,通过[3H]环己基腺苷(CHA)与脑低温切片的结合来研究腺苷A1受体。短暂的全脑缺氧导致海马中[3H]CHA结合位点迅速且持续下调,但新皮层或纹状体中未出现这种情况。先前已表明,给定脑区中腺苷A1受体的密度是决定腺苷抑制作用强度的关键因素。由于这些位点的下调在时间上与短暂缺氧后活动亢进的发作相关,因此有人提出,腺苷神经调节作用强度的降低促成了CA1锥体细胞缺氧后的活动亢进,或许还促成了它们的选择性易损性。