Nikodijević O, Sarges R, Daly J W, Jacobson K A
Laboratory of Bioorganic Chemistry, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.
J Pharmacol Exp Ther. 1991 Oct;259(1):286-94.
The locomotor effects in mice of selective A1 and A2 adenosine agonists, antagonists and combinations of agonists were investigated using a computerized activity monitor. The A2-selective agonist 2-[(2-aminoethylamino)carbonylethylphenylethylamino[-5'-N- ethylcarboxamidoadenosine (APEC), an amine derivative of 2-(carboxyethylphenylethylamino)adenosine-5'-carboxamide, was a more potent locomotor depressant than its amide conjugates. The rank order of potency after i.p. injection for adenosine agonists was 5'-N-ethylcarboxamidoadenosine (NECA) (ED50, 5.8 nmol/kg) greater than APEC (ED50, 25 nmol/kg) greater than N6-cyclohexyladenosine (CHA) (ED50, 270 nmol/kg). An A1-selective, centrally acting, adenosine antagonist, 8-cyclopentyltheophylline (10 mg/kg), completely reversed the locomotor depressant effects of CHA (A1-selective) and NECA (nonselective) at doses of agonists as high as twice the ED50, and shifted the dose-response curves to the right, suggesting a primary involvement of A1 receptors. 8-cyclopentyltheophylline did not affect the depressant effects of APEC at the ED50, consistent with the A2-selectivity of APEC. The locomotor effects of APEC and CHA were completely reversed by theophylline, but not by the peripherally active 8-p-sulfophenyltheophylline, indicating central action of the adenosine agonists. The depressant effects of APEC, but not of NECA or CHA, were reversed significantly by an A2-selective adenosine receptor antagonist, 4-amino-8-chloro-1-phenyl-[1,2,4]triazol[4,3-a]quinoxaline. Low or subthreshold doses of CHA potentiated the depressant effects of APEC. A subthreshold dose of CHA did not alter the depressant effect of NECA, whereas a subthreshold dose of APEC increased the depressant effects of low doses of NECA. Thus, it appears that A1- and A2-selective adenosine agonists have separate central depressant effects, which can be potentiative.(ABSTRACT TRUNCATED AT 250 WORDS)
利用计算机化活动监测仪研究了选择性A1和A2腺苷激动剂、拮抗剂及激动剂组合对小鼠运动的影响。A2选择性激动剂2-[(2-氨基乙氨基)羰基乙基苯乙氨基[-5'-N-乙基羧酰胺腺苷(APEC),即2-(羧基乙基苯乙氨基)腺苷-5'-羧酰胺的胺衍生物,是比其酰胺缀合物更强效的运动抑制剂。腹腔注射后腺苷激动剂的效价顺序为5'-N-乙基羧酰胺腺苷(NECA)(半数有效剂量(ED50),5.8 nmol/kg)大于APEC(ED50,25 nmol/kg)大于N6-环己基腺苷(CHA)(ED50,270 nmol/kg)。一种A1选择性、中枢作用的腺苷拮抗剂8-环戊基茶碱(10 mg/kg),在激动剂剂量高达ED50的两倍时,完全逆转了CHA(A1选择性)和NECA(非选择性)的运动抑制作用,并使剂量-反应曲线右移,提示A1受体起主要作用。8-环戊基茶碱在ED50时不影响APEC的抑制作用,这与APEC的A2选择性一致。APEC和CHA的运动作用被茶碱完全逆转,但未被外周活性的8-对磺基苯基茶碱逆转,表明腺苷激动剂的中枢作用。APEC的抑制作用,但不是NECA或CHA的抑制作用,被A2选择性腺苷受体拮抗剂4-氨基-8-氯-1-苯基-[1,2,4]三唑[4,3-a]喹喔啉显著逆转。低剂量或阈下剂量的CHA增强了APEC的抑制作用。阈下剂量的CHA不改变NECA的抑制作用,而阈下剂量的APEC增加了低剂量NECA的抑制作用。因此,似乎A1和A2选择性腺苷激动剂具有独立的中枢抑制作用,且可能具有增强作用。(摘要截短于250字)