Maskall D D, Zis A P, Lam R W, Clark C M, Kuan A J
Department of Psychiatry, University of British Columbia, Vancouver.
Biol Psychiatry. 1995 Aug 15;38(4):235-9. doi: 10.1016/0006-3223(94)00264-4.
Buspirone-stimulated prolactin release has been employed as an indirect measure of central serotonin activity; however, it is not clear whether serotonergic or dopaminergic systems are responsible for this response. In an attempt to further elucidate the mechanism, we studied the prolactin response to buspirone in eight subjects in the presence of maximal dopaminergic receptor blockade with metoclopramide under placebo-controlled, double-blind conditions. The prolactin response to buspirone in the presence of metoclopramide was not statistically different from that to placebo under the same conditions. The demonstration of further prolactin release by a bolus of thyrotropin-releasing hormone under maximal dopaminergic receptor blockade provided evidence against potential pituitary prolactin depletion by metoclopramide. These results lend further support to a dopaminergic mechanism in buspirone-induced prolactin secretion; therefore, further caution is warranted in interpreting the results of this challenge test as a measure of serotonergic activity in the brain.
丁螺环酮刺激催乳素释放已被用作中枢5-羟色胺活性的一种间接测量方法；然而，尚不清楚是5-羟色胺能系统还是多巴胺能系统介导了这一反应。为进一步阐明其机制，我们在安慰剂对照、双盲条件下，对8名受试者在使用甲氧氯普胺进行最大程度多巴胺能受体阻断的情况下，研究了丁螺环酮刺激后的催乳素反应。在相同条件下，甲氧氯普胺存在时丁螺环酮刺激的催乳素反应与安慰剂刺激的反应在统计学上无差异。在最大程度多巴胺能受体阻断情况下，促甲状腺激素释放激素推注能进一步刺激催乳素释放，这一结果排除了甲氧氯普胺导致垂体催乳素潜在耗竭的可能性。这些结果进一步支持了丁螺环酮诱导催乳素分泌的多巴胺能机制；因此，在将这一激发试验结果解释为大脑5-羟色胺能活性的测量指标时，应更加谨慎。
