Ashe J H, Libet B
Neuropharmacology. 1982 May;21(5):429-31. doi: 10.1016/0028-3908(82)90026-0.
Metoclopramide (MCP) in a sufficiently high concentration (100 microM) induced a large and persisting potentiation of slow-excitatory postsynaptic potentials (s-epsp) and slow-inhibitory postsynaptic potentials (s-epsp) but depressed in fast epsp. This modulatory action of metoclopramide was markedly suppressed by (+)-butaclamol (7 microM) and, to a lesser extent, by spiroperidol (2.5-4 microM). Metoclopramide also possessed weak anti-acetylcholinesterase activity(I50% = 245 microM; measured by Dr N. Inestrosa), but this was shown not to account for the potentiating actions of metoclopramide. Thus, although metoclopramide is a D-2 antagonist, it appears to mimic the D-1 action of dopamine in modulating the slow psps.
甲氧氯普胺（MCP）在足够高的浓度（100微摩尔）时，可诱导慢兴奋性突触后电位（s - epsp）和慢抑制性突触后电位（s - ipsp）出现大幅且持续的增强，但会抑制快兴奋性突触后电位（fast epsp）。甲氧氯普胺的这种调节作用可被（+） - 布他拉莫（7微摩尔）显著抑制，在较小程度上也可被螺哌啶醇（2.5 - 4微摩尔）抑制。甲氧氯普胺还具有较弱的抗乙酰胆碱酯酶活性（I50% = 245微摩尔；由N. Inestrosa博士测定），但已证明这并非甲氧氯普胺增强作用的原因。因此，尽管甲氧氯普胺是一种D - 2拮抗剂，但在调节慢突触后电位时，它似乎模拟了多巴胺的D - 1作用。
