Goldstein J M, Litwin L C, Sutton E B, Malick J B
Life Sci. 1987 Mar 16;40(11):1039-44. doi: 10.1016/0024-3205(87)90565-0.
The effects of SCH 23390 on d-amphetamine-induced suppression of A9 and A10 DA neuronal firing were determined. SCH 23390 potently reversed d-amphetamine on both A9 and A10 DA neurons. Compared to haloperidol, SCH 23390 was 5 times more potent on A9 DA neurons and 20 times more potent on A10 DA neurons. However, the magnitude of the reversal effect was greater with haloperidol than SCH 23390. In addition, haloperidol produced a further increase in firing of both A9 and A10 DA neurons after SCH 23390 maximally increased firing. It was concluded that SCH 23390 has D-2 DA antagonist-like properties, possibly mediated via an interaction at D-1 DA receptors, which may be functionally linked with D-2 DA receptors. The marked potency of SCH 23390 in reversing d-amphetamine could be due to its combined antagonist effects at 5HT2 and D-1 DA receptor sites.
研究了SCH 23390对d-苯丙胺诱导的A9和A10多巴胺能神经元放电抑制的影响。SCH 23390能有效逆转d-苯丙胺对A9和A10多巴胺能神经元的作用。与氟哌啶醇相比，SCH 23390对A9多巴胺能神经元的效力强5倍，对A10多巴胺能神经元的效力强20倍。然而，氟哌啶醇的逆转作用幅度比SCH 23390更大。此外，在SCH 23390使放电达到最大增加后，氟哌啶醇使A9和A10多巴胺能神经元的放电进一步增加。得出的结论是，SCH 23390具有D-2多巴胺拮抗剂样特性，可能通过与D-1多巴胺受体相互作用介导，这可能在功能上与D-2多巴胺受体相关联。SCH 23390逆转d-苯丙胺的显著效力可能归因于其在5HT2和D-1多巴胺受体位点的联合拮抗作用。
