Kelly E, Nahorski S R
Naunyn Schmiedebergs Arch Pharmacol. 1987 May;335(5):508-12. doi: 10.1007/BF00169116.
The effect of dopamine D-2 receptor activation on dopamine D-1 stimulated cyclic AMP accumulation was investigated in slices of rat striatum and limbic forebrain (nucleus accumbens and tuberculum olfactorium). In striatal slices the dose-dependent increase in cyclic AMP accumulation due to dopamine (3-100 mumol/l) was enhanced by selective D-2 receptor blockade using (-)-sulpiride (30 mumol/l). In limbic slices the increase in cyclic AMP due to dopamine (3-50 mumol/l) was unaffected by selective D-2 receptor blockade. The enhancement of cyclic AMP accumulation due to the selective D-1 agonist SKF 38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; 1 mumol/l) in striatal slices was attenuated in the presence of the selective D-2 receptor agonist LY 171555 (quinpirole hydrochloride; 10 mumol/l). This attenuation was in turn blocked by (-)-sulpiride (10 mumol/l). In limbic slices LY 171555 (10 mumol/l) had no effect on SKF 38393 (1 mumol/l) stimulated cyclic AMP accumulation. Conversely muscarine receptor activation, using carbachol (10 mumol/l), attenuated D-1 stimulated cyclic AMP accumulation in both striatum and limbic forebrain. Dopamine D-2 or muscarine receptor stimulation in either striatal or limbic slices did not attenuate cyclic AMP accumulation due to VIP (vasoactive intestinal polypeptide; 0.5 mumol/l), isoprenaline (10 mumol/l) or 2-chloroadenosine (100 mumol/l). This suggests that in striatal slices, D-2 receptors mediate a selective inhibition of D-1 stimulated cyclic AMP accumulation, but that in the limbic forebrain D-2 receptors are unlikely to be coupled to D-1 receptor-linked adenylate cyclase. These data indicate a fundamental difference in the properties of D-2 receptor-effector coupling in these brain regions.
研究了多巴胺D-2受体激活对多巴胺D-1刺激的环磷酸腺苷（cAMP）积累的影响，实验采用大鼠纹状体和边缘前脑（伏隔核和嗅结节）切片。在纹状体切片中，使用（-）-舒必利（30μmol/L）进行选择性D-2受体阻断可增强多巴胺（3 - 100μmol/L）引起的cAMP积累的剂量依赖性增加。在边缘前脑切片中，多巴胺（3 - 50μmol/L）引起的cAMP增加不受选择性D-2受体阻断的影响。在纹状体切片中，选择性D-1激动剂SKF 38393（2,3,4,5-四氢-7,8-二羟基-1-苯基-1H-3-苯并氮杂卓；1μmol/L）引起的cAMP积累增强在选择性D-2受体激动剂LY 171555（盐酸喹吡罗；10μmol/L）存在时减弱。这种减弱又被（-）-舒必利（10μmol/L）阻断。在边缘前脑切片中，LY 171555（10μmol/L）对SKF 38393（1μmol/L）刺激的cAMP积累没有影响。相反，使用卡巴胆碱（10μmol/L）激活毒蕈碱受体可减弱纹状体和边缘前脑中D-1刺激的cAMP积累。在纹状体或边缘前脑切片中，多巴胺D-2或毒蕈碱受体刺激均未减弱血管活性肠肽（VIP；0.5μmol/L）、异丙肾上腺素（10μmol/L）或2-氯腺苷（100μmol/L）引起的cAMP积累。这表明在纹状体切片中，D-2受体介导对D-1刺激的cAMP积累的选择性抑制，但在边缘前脑中，D-2受体不太可能与D-1受体偶联的腺苷酸环化酶偶联。这些数据表明这些脑区中D-2受体-效应器偶联特性存在根本差异。
