Von Lubitz D K, Paul I A, Ji X D, Carter M, Jacobson K A
Molecular Recognition Section, NIH/NIDDK, Bethesda, MD 20892.
Eur J Pharmacol. 1994 Feb 21;253(1-2):95-9. doi: 10.1016/0014-2999(94)90762-5.
The effect of chronic administration of the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) and the adenosine A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX) on N-methyl-D-aspartate (NMDA)-evoked seizures was studied in C57BL/6 mice (20/group). Animals were injected i.p. for 9 days with either 1.0 mg/kg CPA or 1.0 mg/kg CPX followed by 2 injection-free days (the washout period) and subsequent administration of a single dose of 60 mg/kg NMDA. As in our previous study, this dose of NMDA caused clonic/tonic seizures resulting in high (60%) mortality within 3 h after injection of the drug. Despite insignificant changes in seizure latency, chronic pretreatment with CPA increased the incidence of clonic/tonic episodes and end-point mortality. Conversely; chronic exposure to CPX completely eliminated clonic/tonic episodes, significantly increased average survival time, and reduced end-point mortality (P < 0.05). The results indicate that chronic treatment with adenosine A1 receptor antagonist may protect against NMDA-evoked seizures to the same degree as previously observed following a single, acute exposure to CPA. Since the density of adenosine receptor binding sites was unchanged after chronic treatment with either CPX or CPA, it is likely that the mechanism behind the observed protection may rest at the level of second messenger systems coupled to adenosine A1 receptors.
在C57BL/6小鼠(每组20只)中研究了长期给予腺苷A1受体激动剂N6-环戊基腺苷(CPA)和腺苷A1拮抗剂8-环戊基-1,3-二丙基黄嘌呤(CPX)对N-甲基-D-天冬氨酸(NMDA)诱发癫痫发作的影响。动物腹腔注射1.0mg/kg CPA或1.0mg/kg CPX,持续9天,随后有2天停药期(洗脱期),之后给予单剂量60mg/kg NMDA。与我们之前的研究一样,该剂量的NMDA会引起阵挛性/强直性癫痫发作,导致给药后3小时内死亡率较高(60%)。尽管癫痫发作潜伏期变化不显著,但CPA长期预处理会增加阵挛性/强直性发作的发生率和终点死亡率。相反,长期暴露于CPX可完全消除阵挛性/强直性发作,显著延长平均存活时间,并降低终点死亡率(P<0.05)。结果表明,腺苷A1受体拮抗剂的长期治疗可能对NMDA诱发的癫痫发作具有保护作用,其程度与之前单次急性给予CPA后观察到的相同。由于用CPX或CPA长期治疗后腺苷受体结合位点的密度没有变化,观察到的保护作用背后的机制可能在于与腺苷A1受体偶联的第二信使系统水平。