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首页> 外文期刊>The European Journal of Neuroscience >Estrogen regulates adrenal medullary function producing sexual dimorphism in nociceptive threshold and beta-adrenergic receptor-mediated hyperalgesia in the rat.
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Estrogen regulates adrenal medullary function producing sexual dimorphism in nociceptive threshold and beta-adrenergic receptor-mediated hyperalgesia in the rat.

机译：雌激素调节肾上腺髓质功能，在大鼠的伤害感受阈和β-肾上腺素能受体介导的痛觉过敏中产生性二态性。

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Epinephrine produces sexually dimorphic beta(2)-adrenergic receptor-mediated mechanical hyperalgesia, with male rats exhibiting greater hyperalgesia. Because female rats have higher plasma epinephrine levels, and beta-adrenergic receptor sensitivity is affected by chronic exposure to agonists, we tested the hypothesis that this sexual dimorphism is due to epinephrine-induced desensitization of beta(2)-adrenergic receptors. Following gonadectomy, epinephrine hyperalgesia, as measured by the Randall-Selitto paw-withdrawal test, was unchanged in male rats while in females it was increased. Prepubertal male and female rats do not demonstrate sexual dimorphism in either plasma epinephrine level or epinephrine-induced hyperalgesia. Adrenal medullectomy and adrenal denervation both significantly enhanced epinephrine hyperalgesia, but only in females. In contrast, the sexually dimorphic hyperalgesia induced by prostaglandin E(2), another agent that acts directly to sensitize primary afferent nociceptors, was not enhanced by adrenal medullectomy or denervation. Chronic administration of epinephrine in male rats, to produce plasma levels similar to those of gonad-intact females, significantly attenuated epinephrine-induced hyperalgesia, making it similar to that in females. These results strongly support the suggestion that estrogen regulates plasma epinephrine in female rats and differential sensitivity to beta(2)-adrenergic agonists accounts for the sexual dimorphism in epinephrine-induced hyperalgesia. Unexpectedly, regulation of adrenal medullary function by estrogen was also found to modulate baseline nociceptive threshold such that females had a lower nociceptive threshold.
机译：肾上腺素产生性双态性β（2）-肾上腺素能受体介导的机械性痛觉过敏，雄性大鼠表现出更大的痛觉过敏。因为雌性大鼠具有更高的血浆肾上腺素水平，并且β-肾上腺素受体敏感性受慢性暴露于激动剂的影响，所以我们测试了这种性二态性是由于肾上腺素引起的β（2）-肾上腺素受体脱敏的假设。在性腺切除术后，通过Randall-Selitto爪缩回试验测量的肾上腺素痛觉过敏在雄性大鼠中没有变化，而在雌性大鼠中则有所增加。青春期前的雄性和雌性大鼠在血浆肾上腺素水平或肾上腺素诱导的痛觉过敏中均未表现出性二态性。肾上腺髓质切除术和肾上腺去神经都明显增强肾上腺素的痛觉过敏，但仅在女性中。相比之下，肾上腺髓质切除术或去神经不能增强前列腺素E（2）引起的性二形痛觉过敏，前列腺素E（2）是另一种直接使原发传入伤害感受器敏感的药物。长期给予雄性大鼠肾上腺素以产生与性腺完整的雌性相似的血浆水平，可显着减轻肾上腺素引起的痛觉过敏，使其与雌性相似。这些结果强烈支持雌激素调节雌性大鼠血浆肾上腺素的建议，对β（2）-肾上腺素能激动剂的敏感性差异解释了肾上腺素诱导的痛觉过敏的性二态性。出乎意料的是，还发现雌激素对肾上腺髓质功能的调节可调节基线伤害阈值，从而使女性的伤害阈值较低。

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