Nagasawa H, Araki T, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Neuroreport. 1994 Jul 21;5(12):1453-6. doi: 10.1097/00001756-199407000-00011.
Chronological changes of adenosine A1 receptor binding of the rat brain were determined by in vitro [3H]cyclohexyladenosine (CHA) autoradiography after 90 min of middle cerebral artery (MCA) occlusion and after such occlusion followed by different periods of recirculation. One day after the ischaemia, [3H]CHA binding sites decreased significantly in the cerebral cortex (p < 0.05) and lateral segment of the caudate putamen (p < 0.01), both supplied by the occluded MCA; thereafter, the binding sites decreased progressively in those ischaemic foci. On the contrary, there was no alteration on day 1, but 3 days after ischaemic insult, a significant decrease of [3H]CHA binding sites was first detected in the ipsilateral thalamus and the substantia nigra, both areas which had not been directly affected by the original ischaemic insult. This post-ischaemic delayed phenomenon observed in the thalamus and the substantia nigra developed concurrently with 45Ca accumulation, which was studied in our previous study. Based on the present study, alteration of adenosine A1 receptor binding activities is involved not only in the ischaemic foci, but also in the remote areas associated neuroanatomically with the ischaemic foci. We suggest that multi-focal post-ischaemic alterations of adenosine A1 binding activities may exacerbate clinical symptoms of patients at a chronic stage of stroke.
通过体外[3H]环己基腺苷(CHA)放射自显影术,在大脑中动脉(MCA)闭塞90分钟后以及闭塞后不同时间段的再灌注后,测定大鼠脑内腺苷A1受体结合的时间变化。缺血后1天,在由闭塞的MCA供血的大脑皮质(p < 0.05)和尾状壳核外侧段(p < 0.01),[3H]CHA结合位点显著减少;此后,这些缺血灶中的结合位点逐渐减少。相反,在缺血损伤后1天没有变化,但在缺血损伤后3天,首次在同侧丘脑和黑质中检测到[3H]CHA结合位点显著减少,这两个区域未直接受到原始缺血损伤的影响。在丘脑和黑质中观察到的这种缺血后延迟现象与45Ca积累同时发生,45Ca积累在我们之前的研究中已进行过研究。基于本研究,腺苷A1受体结合活性的改变不仅涉及缺血灶,还涉及与缺血灶在神经解剖学上相关的远隔区域。我们认为,腺苷A1结合活性的多灶性缺血后改变可能会加重中风慢性期患者的临床症状。