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戊四氮诱发癫痫发作后不同小鼠脑区A1腺苷受体的改变,但癫痫突变小鼠“蹒跚”中未出现这种改变。

Alterations of A1 adenosine receptors in different mouse brain areas after pentylentetrazol-induced seizures, but not in the epileptic mutant mouse 'tottering'.

作者信息

Angelatou F, Pagonopoulou O, Kostopoulos G

机构信息

Department of Physiology, University of Patras, Medical School, Greece.

出版信息

Brain Res. 1990 Nov 26;534(1-2):251-6. doi: 10.1016/0006-8993(90)90136-y.

Abstract

Single and repeated Pentylentetrazol (PTZ)-induced convulsions are associated with significant changes of A1 adenosine receptors (detected using the radioligand [3H]cyclohexyladenosine, [3H]CHA) in 4 different brain areas of the mouse, namely cortex, hippocampus, cerebellum and striatum. In hippocampus and cerebellum, a rapid increase in [3H]CHA binding, by 26% and 30% respectively, was observed 1 h after a single PTZ convulsion. In striatum, on the contrary, a significant decrease by 30% in [3H]CHA binding was seen, whereas in cortex no significant change could be detected. After daily repeated PTZ convulsions, a significant increase of A1 receptors by 26% appeared also in cortex, while the changes of A1 receptors observed in the other brain areas after a single PTZ convulsion were maintained in almost the same range. All the alterations observed were due to changes of the total number of A1 receptors (Bmax) without changes in receptor affinity (Kd). A significant increase in the latency of PTZ seizure (time between the PTZ-injection and the beginning of the seizure) was also observed after repeated PTZ-induced convulsions at the time when the changes in A1 adenosine receptors were noted. Considered together, these results provide further evidence for an A1 receptor-mediated modulation of seizure susceptibility and indicate that specific brain areas may play different roles in this modulation. The binding of [3H]CHA to membranes from different cortical and subcortical areas of the epileptic mutant mouse 'tottering' was not different from that in control animals.

摘要

单次和重复戊四氮(PTZ)诱导的惊厥与小鼠4个不同脑区(即皮层、海马、小脑和纹状体)中A1腺苷受体(使用放射性配体[3H]环己基腺苷,[3H]CHA检测)的显著变化有关。在海马和小脑中,单次PTZ惊厥1小时后,观察到[3H]CHA结合分别快速增加26%和30%。相反,在纹状体中,[3H]CHA结合显著下降30%,而在皮层中未检测到显著变化。每日重复PTZ惊厥后,皮层中A1受体也显著增加26%,而单次PTZ惊厥后在其他脑区观察到的A1受体变化维持在几乎相同的范围内。观察到的所有改变均归因于A1受体总数(Bmax)的变化,而受体亲和力(Kd)未改变。在注意到A1腺苷受体变化时,重复PTZ诱导的惊厥后,还观察到PTZ癫痫发作潜伏期(PTZ注射与发作开始之间的时间)显著增加。综合考虑,这些结果为A1受体介导的癫痫易感性调节提供了进一步证据,并表明特定脑区在这种调节中可能发挥不同作用。癫痫突变小鼠“蹒跚”不同皮层和皮层下区域膜上[3H]CHA的结合与对照动物无异。

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