Whitcomb K, Lupica C R, Rosen J B, Berman R F
Department of Psychology, Wayne State University, Detroit, MI 48202.
Epilepsy Res. 1990 Aug;6(3):171-9. doi: 10.1016/0920-1211(90)90070-c.
The actions of adenosine in modulating amygdala kindling were examined using the stable adenosine analog 5'-N'-ethylcarboxamidoadenosine (NECA) and caffeine, an adenosine antagonist. Systemically administered NECA was found to significantly reduce the rate of postictal spiking and to significantly increase the duration of postictal EEG depression in amygdala kindled rats. In contrast, systemically administered caffeine significantly increased kindled seizure duration and reduced the duration of postictal EEG depression. Systemic administration of the methylxanthine derivative, 8-sulfophenyl theophylline (8-PST), failed to block the effects of NECA on kindling. Since systemically administered 8-PST blocks peripheral adenosine receptors, but has only limited CNS activity, the effects of NECA appear to be centrally mediated. These observations further demonstrate a role for adenosine in postictal phenomena and support the hypothesis that a release of endogenous adenosine contributes to the termination of ongoing seizure activity.
使用稳定的腺苷类似物5'-N'-乙基羧基酰胺腺苷（NECA）和腺苷拮抗剂咖啡因，研究了腺苷在调节杏仁核点燃中的作用。结果发现，全身给药的NECA可显著降低杏仁核点燃大鼠的发作后棘波发放率，并显著增加发作后脑电图抑制的持续时间。相反，全身给药的咖啡因可显著增加点燃性癫痫发作的持续时间，并缩短发作后脑电图抑制的持续时间。甲基黄嘌呤衍生物8-磺基苯基茶碱（8-PST）全身给药未能阻断NECA对点燃的影响。由于全身给药的8-PST可阻断外周腺苷受体，但中枢神经系统活性有限，因此NECA的作用似乎是由中枢介导的。这些观察结果进一步证明了腺苷在发作后现象中的作用，并支持内源性腺苷释放有助于终止正在进行的癫痫活动这一假说。
