Dragunow M
Department of Pharmacology, School of Medicine, University of Auckland, New Zealand.
Pharmacol Biochem Behav. 1990 Aug;36(4):751-5. doi: 10.1016/0091-3057(90)90072-p.
The mechanism of action of aminophylline in prolonging seizures was tested in amygdala-kindled rats. Aminophylline prolonged the afterdischarge duration of kindled seizures. This seizure-prolonging action of aminophylline was strongly antagonized by the adenosine A1 agonist cyclohexyladenosine and partially antagonized by the benzodiazepine partial agonist RO 15-1788. However, the specific benzodiazepine antagonist CGS 8216 did not affect the seizure-prolonging action of aminophylline. Also, the potent anticonvulsant effect of diazepam on kindled seizures, which was completely antagonized by CGS 8216, was unaffected by aminophylline. Furthermore, a range of benzodiazepine inverse agonists, GABA antagonists, phosphodiesterase inhibitors and xanthines did not prolong afterdischarge durations. These results demonstrate that the seizure-prolonging action of aminophylline is due to block of A1 adenosine receptors since it is prevented by adenosine A1 agonists.
在杏仁核点燃大鼠中测试了氨茶碱延长癫痫发作的作用机制。氨茶碱延长了点燃性癫痫发作的放电后持续时间。氨茶碱的这种癫痫发作延长作用被腺苷A1激动剂环己基腺苷强烈拮抗,被苯二氮䓬部分激动剂RO 15 - 1788部分拮抗。然而,特异性苯二氮䓬拮抗剂CGS 8216不影响氨茶碱的癫痫发作延长作用。此外,地西泮对点燃性癫痫发作的强效抗惊厥作用完全被CGS 8216拮抗,但不受氨茶碱影响。此外,一系列苯二氮䓬反向激动剂、GABA拮抗剂、磷酸二酯酶抑制剂和黄嘌呤均未延长放电后持续时间。这些结果表明,氨茶碱的癫痫发作延长作用是由于A1腺苷受体的阻断,因为它被腺苷A1激动剂所阻止。