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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The effect of anandamide on prolactin secretion is modulated by estrogen.
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The effect of anandamide on prolactin secretion is modulated by estrogen.

机译：雄激素对催乳激素分泌的影响是由雌激素调节的。

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Recent research has revealed that endogenous cannabinoid receptors (CB1 and CB2) react with the active ingredient of marijuana, Delta(9)-tetrahydrocannabinol. Two endogenous ligands activate these receptors. The principal one, anandamide (AEA), activates CB1. AEA and CB1 are localized to various neurons within the brain. Because Delta(9)-tetrahydrocannabinol inhibited prolactin (Prl) secretion following its intraventricular injection into male rats, we hypothesized that AEA would have a similar effect. Estrogen modifies many hormonal responses and is known to increase Prl secretion. Therefore, we hypothesized that responses to intraventricular AEA would change depending on the gonadal steroid environment. Consequently, we evaluated the effects of lateral cerebral ventricular microinjection of AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed (OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect in OVX females, and increased Prl in OVX-E rats. The results were at least partially mediated by changes in dopaminergic turnover, altering the inhibitory dopaminergic control of Prl release by the anterior pituitary gland. Thus, dopamine turnover was increased in the male rats and decreased significantly in OVX and in OVX-E rats. The changes in Prl may be caused not only by altered dopamine input to the anterior pituitary gland but also by effects of AEA on other transmitters known to alter Prl release. Importantly, in OVX-E rats, the elevated Prl release and the response to AEA were blocked by the AEA antagonist, indicating that AEA is a synaptic transmitter released from neurons that decrease inhibitory control of Prl release.
机译：最近的研究表明，内源性大麻素受体（CB1和CB2）与大麻的活性成分Delta（9）-四氢大麻酚反应。两个内源性配体激活这些受体。最主要的一种，是anandamide（AEA），可激活CB1。 AEA和CB1定位于大脑内的各种神经元。因为Delta（9）-四氢大麻酚对雄性大鼠进行脑室内注射后抑制了催乳素（Prl）的分泌，所以我们假设AEA具有类似的作用。雌激素可改变许多激素反应，并已知会增加Prl分泌。因此，我们假设对脑室内AEA的反应将根据性腺类固醇的环境而变化。因此，我们评估了AEA（20 ng）侧脑室显微注射对雄性，去卵巢（OVX）和雌激素致敏（OVX-E）大鼠的影响。 AEA降低雄性大鼠血浆Prl，对OVX雌性影响不大，而OVX-E大鼠血浆Prl增加。结果至少部分地由多巴胺能转换的改变介导，改变了垂体前叶对Prl释放的抑制性多巴胺能控制。因此，在雄性大鼠中多巴胺转换增加，在OVX和OVX-E大鼠中多巴胺转换显着降低。 Prl的变化不仅可能是由于垂体前叶多巴胺输入的改变，还可能是由于AEA对其他已知改变Prl释放的递质的影响。重要地，在OVX-E大鼠中，AEA拮抗剂阻断了升高的PrI释放和对AEA的应答，表明AEA是从神经元释放的突触递质，其降低了对Prl释放的抑制控制。

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