Lack of catecholamine involvement in the increased luteinizing hormone release due to blockade of kappa-opioid receptors in the medial basal hypothalamus during midpregnancy in the rat.
Lack of catecholamine involvement in the increased luteinizing hormone release due to blockade of kappa-opioid receptors in the medial basal hypothalamus during midpregnancy in the rat.
复制标题
由于大鼠妊娠中期下丘脑内侧基底的κ阿片受体被阻断，黄体生成激素释放增加中缺乏儿茶酚胺的参与。
DOI：
10.1016/0006-8993(94)90920-2
复制
发表时间：
1994
期刊：
影响因子：
2.9
通讯作者：
Gallo,RV
中科院分区：
文献类型：
--
作者：
Zhen,S;Gallo,RV
用nor-binaltorphimine（nor-BNI）阻断内侧基底下丘脑（MBH）中的κ-阿片受体可刺激大鼠妊娠中期促黄体生成素（LH）的释放[48]。本研究的目的是确定去甲肾上腺素（NE）或多巴胺（DA）是否介导LH对妊娠第13-17天MBH κ-阿片受体阻断的反应。进行了两个实验。第一种方法是采用推挽式灌注结合HPLC监测MBH中NE的体内释放，这些NE释放是对（a）人工CSF，然后是含有nor-BNI（40 μg/h）的CSF，（B）CSF中的去甲丙咪嗪（去甲丙咪嗪，NE再摄取阻断剂，10 μM），然后是去甲丙咪嗪，以及（c）去甲丙咪嗪，然后是去甲丙咪嗪+ nor-BNI的反应。以12分钟的间隔采集血液样品，同时采集推拉灌注液样品。用放射免疫法测定血浆LH水平。Nor-BNI显着增加LH的释放相比，单独的CSF，但灌注液NE是不可检测的灌注期。然而，在这些大鼠中用含有100 mM K+的CSF灌注显著增加灌注液NE水平，表明去甲肾上腺素能神经末梢存在于MBH的灌注部位。脑脊液中加入异丙肾上腺素可显著增加灌流液NE水平，但对LH释放无明显影响。Nor-BNI + BNI灌注增加LH分泌类似于单独的Nor-BNI，但与单独的BNI灌注相比，MBH灌注液NE水平没有额外增加。在第二个实验中，在用NE合成抑制剂弗拉-63（25 mg/kg，s.c.），α-肾上腺素能受体阻断剂酚妥拉明（5 mg/kg，i. v.），DA受体拮抗剂d-丁他拉莫（1 mg/kg，s.c.），或车辆。这些药物治疗均不影响nor-BNI灌注MBH期间LH释放的增加。结果表明，NE和DA均不介导孕中期大鼠MBH κ-阿片受体阻断后LH释放的增加。
Blockade of κ-opioid receptors in the medial basal hypothalamus (MBH) with nor-binaltorphimine (nor-BNI) stimulates luteinizing hormone (LH) release during midpregnancy in the rat [48]. The objective of this study was to determine whether norepinephrine (NE) or dopamine (DA) mediates the LH response to blockade of MBH κ-opioid receptors on days 13–17 of pregnancy in the rat. Two experiments were conducted. In the first, push-pull perfusion in conjunction with HPLC was used to monitor in vivo NE release in the MBH occuring in response to (a) artificial CSF followed by CSF containing nor-BNI (40 μg/h), (b) desipramine (DMI, a NE reuptake blocker, 10 μM) in CSF followed by DMI, and (c) DMI followed by DMI + nor-BNI. Blood samples were taken at 12 min intervals concurrent with push-pull perfusate samples. Plasma LH levels were determined by RIA. Nor-BNI significantly increased LH release compared to CSF alone, but perfusate NE was undetectable in either perfusion period. However, perfusion with CSF containing 100 mM K+in these rats markedly increased perfusate NE levels, indicating noradrenergic nerve terminals were present at the perfusion sites in the MBH. Addition of DMI to the CSF significantly increased perfusate NE levels, but produced no changhe in LH release. Nor-BNI + DMI perfusion increased LH secretion similar to nor-BNI alone, but produced no additional increase in MBH perfusate NE levels compared to perfusion with DMI alone. In the second experiment, push-pull perfusion in the MBH with nor-BNI was done in rats pretreated either with the NE synthesis inhibitor FLA-63 (25 mg/kg, s.c.), the α-adrenergic receptor blocker phentolamine (5 mg/kg, i.v.), the DA receptor antagonist d-butaclamol (1 mg/kg, s.c.), or vehicle. None of these drug treatments affected the increased LH release occuring during MBH perfusion with nor-BNI. The present results demonstrate that neither NE nor DA mediates the increased LH release occuring in response to blockade of κ-opioid receptors in the MBH during midpregnancy in the rat.