Macgregor D G, Stone T W
Dept. of Pharmacology, University of Glasgow, UK.
Brain Res. 1994 May 2;644(2):339-42. doi: 10.1016/0006-8993(94)91700-0.
The adenosine A1 receptor selective antagonist 1,3-dipropyl-8-cyclopentylxanthine (CPX) has been administered systemically to rats together with the neurotoxin kainic acid. At the lower doses of CPX tested, 10 and 50 micrograms/kg, which were sufficient to prevent the neuroprotective activity of exogenous agonists, there was no exacerbation of the neuronal damage. At 250 micrograms/kg, some enhancement of damage was found, which was also produced by 8-(p-sulphophenyl)theophylline, a non-selective xanthine which does not cross the blood-brain barrier. The results are consistent with the involvement of a central A1 receptor in the neuroprotective activity of purines, and suggest that blockade of a peripheral adenosine receptor, possibly of the A2 type, may increase neuronal damage.
已将腺苷A1受体选择性拮抗剂1,3 - 二丙基 - 8 - 环戊基黄嘌呤（CPX）与神经毒素海藻酸一起全身给药于大鼠。在所测试的较低剂量的CPX（10和50微克/千克）下，这足以阻止外源性激动剂的神经保护活性，未发现神经元损伤加剧。在250微克/千克时，发现损伤有所增强，8 - （对 - 磺基苯基）茶碱也会产生这种增强作用，8 - （对 - 磺基苯基）茶碱是一种不穿过血脑屏障的非选择性黄嘌呤。这些结果与中枢A1受体参与嘌呤的神经保护活性一致，并表明阻断外周腺苷受体（可能是A2型）可能会增加神经元损伤。
