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氨茶碱与点燃式癫痫发作

Aminophylline and kindled seizures.

作者信息

Albertson T E, Stark L G, Joy R M, Bowyer J F

出版信息

Exp Neurol. 1983 Sep;81(3):703-13. doi: 10.1016/0014-4886(83)90337-0.

Abstract

The effects of aminophylline on amygdaloid and cortically kindled rats was studied. Rats implanted with chronic amygdaloid electrodes received either saline or 150 mg/kg, i.p., aminophylline 20 min prior to their first stimulation. On the first stimulation, aminophylline-treated rats had dramatically longer afterdischarge durations and more severe seizure ranks. When fully kindled, the animals were retested with saline or aminophylline. Again, the aminophylline-treated animals had longer afterdischarge durations than the saline-treated rats. In a second experiment, fully amygdaloid kindled rats were pretreated with various doses of aminophylline and stimulated 20 min later. With suprathreshold stimulation, a dose-dependent increase was noted in the afterdischarge duration. During seizure threshold determinations, aminophylline pretreatment markedly prolonged afterdischarge durations without significantly changing seizure severity or threshold. When animals were treated with the adenosine agonist, 2-chloroadenosine, prior to kindled amygdaloid stimulation, the elicited afterdischarge was shortened. The effect was antagonized where treatment with both 2-chloroadenosine and aminophylline occurred prior to amygdaloid stimulation. Rats with neocortical electrodes were also exposed to various doses of aminophylline while in a stable, partially developed kindled stage and again when fully kindled. At both stages, afterdischarge duration was increased by aminophylline in a dose-dependent manner. The partially developed, cortically kindled animals were more responsive to aminophylline than were those fully kindled and they tended to have greater increases in afterdischarge duration and seizure rank. These data demonstrate that aminophylline acts to prolong afterdischarges elicited at various stages of kindling from both amygdaloid and cortical sites.

摘要

研究了氨茶碱对杏仁核点燃和皮层点燃大鼠的影响。植入慢性杏仁核电极的大鼠在首次刺激前20分钟腹腔注射生理盐水或150mg/kg氨茶碱。在首次刺激时,氨茶碱处理的大鼠的放电后持续时间显著延长,癫痫等级更严重。当完全点燃后,用生理盐水或氨茶碱对动物进行重新测试。同样,氨茶碱处理的动物的放电后持续时间比生理盐水处理的大鼠更长。在第二个实验中,对完全杏仁核点燃的大鼠用不同剂量的氨茶碱进行预处理,20分钟后进行刺激。在阈上刺激时,观察到放电后持续时间呈剂量依赖性增加。在癫痫阈值测定期间,氨茶碱预处理显著延长了放电后持续时间,而癫痫严重程度或阈值没有显著变化。当在点燃的杏仁核刺激前用腺苷激动剂2-氯腺苷处理动物时,诱发的放电后时间缩短。当在杏仁核刺激前同时用2-氯腺苷和氨茶碱处理时,这种作用被拮抗。植入新皮层电极的大鼠在稳定的部分发展的点燃阶段以及完全点燃时也接受不同剂量的氨茶碱。在两个阶段,氨茶碱均以剂量依赖性方式增加放电后持续时间。部分发展的皮层点燃动物比完全点燃的动物对氨茶碱更敏感,它们的放电后持续时间和癫痫等级增加往往更大。这些数据表明,氨茶碱的作用是延长在杏仁核和皮层部位点燃的各个阶段诱发的放电后时间。

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