Jackisch R, Moll S, Feuerstein T J, Hertting G
Naunyn Schmiedebergs Arch Pharmacol. 1985 Aug;330(2):105-13. doi: 10.1007/BF00499902.
3H-Noradrenaline release in the rabbit hippocampus and its possible modulation via presynaptic dopamine receptors was studied. Hippocampal slices were preincubated with 3H-noradrenaline, continuously superfused in the presence of cocaine (30 mumol/l) and subjected to electrical field stimulation. The electrically evoked tritium overflow from the slices was reduced by 0.1 and 1 mumol/l dopamine and apomorphine, but significantly enhanced by 10 mumol/l apomorphine or by 0.1 and 1 mumol/l bromocriptine. If the alpha 2-adrenoceptor antagonist yohimbine (0.1 mumol/l) was present throughout superfusion, the inhibitory effects of dopamine and apomorphine were more pronounced and even 10 mumol/l apomorphine and 1 mumol/l bromocriptine inhibited noradrenaline release. Qualitatively similar observations were made in the presence of another alpha 2-antagonist, idazoxane (0.1 mumol/l). In the presence of the D2-receptor antagonist domperidone (0.1 mumol/l) the inhibitory effects of dopamine were almost abolished, whereas both apomorphine (greater than 1 mumol/l) and bromocriptine (greater than 0.01 mumol/l) greatly facilitated noradrenaline release. The D2-receptor agonist LY 171555 (0.1 and 1 mumol/l) significantly reduced the evoked noradrenaline release whereas the D1-selective agonist SK & F 38393 was ineffective at similar concentrations. The effects of LY 171555 were abolished in the presence of domperidone (0.1 mumol/l) but remained unchanged in the presence of yohimbine or idazoxane (0.1 mumol/l, each). At 1 mumol/l the D2-receptor antagonists domperidone and (-)sulpiride significantly increased the evoked noradrenaline release by about 10%. However, at this concentration, domperidone (but not (-)sulpiride) affected also basal tritium outflow. Bulbocapnine and the preferential D1-receptor antagonists SCH 23390 enhanced the evoked noradrenaline release already at 0.1 mumol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了家兔海马中3H-去甲肾上腺素的释放及其通过突触前多巴胺受体的可能调节。将海马切片与3H-去甲肾上腺素预孵育，在可卡因（30μmol/L）存在下持续灌流，并进行电场刺激。0.1和1μmol/L的多巴胺及阿扑吗啡可使切片中电诱发的氚溢出减少，但10μmol/L阿扑吗啡或0.1和1μmol/L溴隐亭可使其显著增加。如果在整个灌流过程中加入α2-肾上腺素能受体拮抗剂育亨宾（0.1μmol/L），多巴胺和阿扑吗啡的抑制作用会更明显，甚至10μmol/L阿扑吗啡和1μmol/L溴隐亭也会抑制去甲肾上腺素的释放。在另一种α2-拮抗剂伊达唑烷（0.1μmol/L）存在下也观察到了定性相似的结果。在D2-受体拮抗剂多潘立酮（0.1μmol/L）存在下，多巴胺的抑制作用几乎被消除，而阿扑吗啡（大于1μmol/L）和溴隐亭（大于0.01μmol/L）则极大地促进了去甲肾上腺素的释放。D2-受体激动剂LY 171555（0.1和1μmol/L）显著降低了诱发的去甲肾上腺素释放，而D1-选择性激动剂SK&F 38393在相似浓度下无效。LY 171555的作用在多潘立酮（0.1μmol/L）存在下被消除，但在育亨宾或伊达唑烷（各0.1μmol/L）存在下保持不变。1μmol/L时，D2-受体拮抗剂多潘立酮和（-）舒必利可使诱发的去甲肾上腺素释放显著增加约10%。然而，在此浓度下，多潘立酮（而非（-）舒必利）也影响基础氚流出。千金藤素和优先的D1-受体拮抗剂SCH 23390在0.1μmol/L时就增强了诱发的去甲肾上腺素释放。（摘要截取自250字）
