Mu and kappa opioid receptor expression in the mediobasal hypothalamus and effectiveness of selective antagonists on prolactin release during lactation.
Mu and kappa opioid receptor expression in the mediobasal hypothalamus and effectiveness of selective antagonists on prolactin release during lactation.
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DOI：
10.1016/j.neuroscience.2009.12.066
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发表时间：
2010-03-17
期刊：
影响因子：
3.3
通讯作者：
Arbogast, L. A.
中科院分区：
文献类型：
--
作者：
Tavakoli-Nezhad, M.;Arbogast, L. A.
内源性阿片肽参与泌乳期间催乳素的释放，部分是通过降低结节漏斗多巴胺能（TIDA）神经元的活动。μ和κ阿片受体在剥夺4- 5 h后吸吮诱导的催乳素升高中均起作用。本研究旨在观察μ阿片受体拮抗剂β-funaltorphamine（β-FNA）和κ阿片受体拮抗剂nor-binaltorphimine（nor-BNI）对幼鼠剥夺18 h后泌乳大鼠催乳素分泌和TIDA神经元活动的影响。与幼仔分离4 h后，16 μg nor-BNI和5 μg β-FNA可消除吸吮诱导的催乳素升高，与茎正中隆起（SME）中二羟苯乙酸（DOPAC）：多巴胺比例增加一致。然而，在18小时幼仔分离后，这些相同剂量的nor-BNI和β-FNA没有改变SME中的催乳素峰或DOPAC：多巴胺比率。需要更高剂量的nor-BNI（32 μg）和β-FNA（10 μg）来抑制哺乳诱导的催乳素分泌。β-FNA（10 μg）增加SME中DOPAC：多巴胺的比例，而nor-BNI（32 μg）治疗没有影响。剥夺4 h后，下丘脑内侧基底核μ和κ阿片受体mRNA水平与哺乳对照组相似，但剥夺18 h后增加1.4倍。这些数据支持参与内源性阿片系统在吸吮诱导的催乳素上升后，幼犬剥夺的时间延长（18小时），以及较短的（4小时）幼犬剥夺期以前报道。TIDA神经元活动的抑制可能在μ阿片受体输入中起作用，从而在4 h和18 h分离后的吮吸诱导的催乳素升高中起作用，而非多巴胺能输入在18 h剥夺后与κ阿片受体有关。下丘脑中基底核μ和κ阿片受体基因表达增加可能导致阿片受体拮抗剂阻断18 h剥夺后吮吸诱导的催乳素释放的有效性降低。
Endogenous opioid peptides are involved in prolactin release during lactation, in part by decreasing tuberoinfundibular dopaminergic (TIDA) neuronal activity. Both μ and κ opioid receptors have a role in the suckling-induced prolactin rise after 4-5h pup deprivation. The aim of this study was to investigate effects of μ opioid receptor antagonist, β-funaltrexamine (β-FNA), and κ opioid receptor antagonist, nor-binaltorphimine (nor-BNI), on prolactin secretion and TIDA neuronal activity in lactating rats after 18h pup deprivation. After 4h separation from pups, the suckling-induced prolactin rise was abolished by 16 μg nor-BNI and 5 μg β-FNA, coincident with increased dihydroxyphenylacetic acid (DOPAC):dopamine ratio in the stalk-median eminence (SME). However, after 18h pups separation, these same doses of nor-BNI and β-FNA did not alter the prolactin surge or DOPAC:dopamine ratios in the SME. Higher doses of nor-BNI (32 μg) and β-FNA (10 μg) were required to inhibit suckling-induced prolactin secretion. β-FNA (10 μg) increased the DOPAC:dopamine ratio in the SME, whereas nor-BNI (32 μg) treatment had no effect. The μ and κ opioid receptor mRNA levels in the mediobasal hypothalamus were similar to suckled control rats after 4h pup deprivation, but increased 1.4-fold after 18h pup deprivation. These data support involvement of endogenous opioidergic systems in the suckling-induced prolactin rise after a prolonged (18h) period of pup deprivation, as well as the shorter (4h) pup deprivation period previously reported. Suppression of TIDA neuronal activity likely played a part in μ opioid receptor input to the suckling-induced prolactin rise after both 4h and 18h separation, whereas non-dopaminergic input was implicated with κ opioid receptors after 18h pup deprivation. Increased μ and κ opioid receptors gene expression in the mediobasal hypothalamus may contribute to reduced effectiveness of opioid receptor antagonists to block suckling-induced prolactin release after 18h pup deprivation.
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