Brann D W, Mahesh V B
Department of Physiology and Endocrinology, Medical College of Georgia, Augusta.
Neuroendocrinology. 1991 Jan;53(1):107-10. doi: 10.1159/000125706.
The role of endogenous excitatory amino acid neurotransmission in the regulation of progesterone and triamcinolone acetonide-induced LH and FSH release was examined. Estrogen-primed ovariectomized rats were utilized in this study. Progesterone or triamcinolone acetonide (1 mg/kg body weight) treatment led to a highly significant elevation of serum LH and FSH levels 5 h later. Treatment with the selective noncompetitive NMDA receptor antagonist, MK801, had no effect on serum LH and FSH levels when compared to estrogen controls. However, MK801 administered 1 h prior to progesterone or triamcinolone acetonide administration completely blocked their ability to induce LH and FSH surges. These studies demonstrate for the first time the involvement of endogenous excitatory amino acid neurotransmission in the mediation of progesterone and corticosteroid-induced LH and FSH surges.
研究了内源性兴奋性氨基酸神经传递在孕酮和曲安奈德诱导促黄体生成素（LH）和促卵泡生成素（FSH）释放调节中的作用。本研究使用了雌激素预处理的去卵巢大鼠。孕酮或曲安奈德（1毫克/千克体重）处理5小时后导致血清LH和FSH水平显著升高。与雌激素对照组相比，选择性非竞争性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK801处理对血清LH和FSH水平无影响。然而，在给予孕酮或曲安奈德前1小时给予MK801可完全阻断它们诱导LH和FSH激增的能力。这些研究首次证明内源性兴奋性氨基酸神经传递参与了孕酮和皮质类固醇诱导的LH和FSH激增的介导过程。
