Opioids act centrally to modulate stress-induced decrease in luteinizing hormone in the rat.
Opioids act centrally to modulate stress-induced decrease in luteinizing hormone in the rat.
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阿片类药物的主要作用是调节应激引起的大鼠黄体生成激素的减少。
作者：
Felice Petraglia;W. Vale;C. Rivier
由于内源性阿片肽（EOP）和CRF在应激时被激活，并在中央注射时降低LH水平，我们已经探索了这些肽在应激诱导的LH分泌抑制中的作用。下丘脑中存在三种阿片肽系统[即内啡肽（END）、脑啡肽（enkephalin）、啡啡肽（DYN）]，作用于不同的阿片受体亚型（即mu、delta、kappa）。我们首先评估了哪些EOP可能与应激诱导的LH水平下降有关。采用EOP免疫中和和阿片受体药物阻断的方法，逆转了去势雄性大鼠不可避免的间歇性足电引起的LH下降。抗-END和抗dyn -a血清（脑室内[icv]）或预处理β -END拮抗剂β -人END-(6-31)(2和5 nmol， icv)，或预处理kappa拮抗剂Mr1452 MS和Mr2266 BS (10 mg/kg BW, ip)，可逆转电刺激诱导的LH浓度降低。β -富纳曲胺（β - fna）是一种不可逆的mu 1-阿片受体拮抗剂，可部分阻断应激对LH水平的抑制作用。抗脑啡肽被动免疫和δ -阿片受体拮抗剂ICI 154,129（10和100 nmol， icv）预处理均未改变应激效应。然后，我们评估了哪些内源性阿片配体和/或受体可能介导了对2 nmol绵羊CRF注射后LH水平的抑制作用。抗β -END血清和β -人END-(6-31)逆转了crf诱导的LH浓度下降，而β - fna仅部分有效。抗dyn -a和抗enk血清、kappa和δ拮抗剂不能阻止中枢接受CRF大鼠LH水平的下降。这些数据表明，应激诱导的LH分泌抑制涉及通过mu/epsilon-或kappa-阿片受体刺激β - end和DYN-A系统，中央给药CRF诱导的循环LH水平下降可能是通过激活β - end系统介导的。因此，中枢CRF/ β - end通路的激活可能在应激诱导的生殖功能抑制中发挥重要作用。
Because endogenous opioid peptides (EOP) and CRF are activated during stress and decrease LH levels when injected centrally, we have explored the roles of these peptides in the stress-induced inhibition of LH secretion. Three opioid peptide systems [i.e. endorphin (END), enkephalin, dynorphin (DYN)], are present in the hypothalamus, acting on different opiate receptor subtypes (i.e. mu, delta, kappa). We first evaluated which EOP might be involved in the stress-induced decrease of LH levels. Immunoneutralization of EOP and pharmacological blockade of opiate receptors were used to reverse the decrease in LH induced by inescapable intermittent footshock in castrated male rats. Anti-beta-END and anti-DYN-A serum (intracerebroventricularly [icv]) or pretreatment with beta-END antagonist, beta-human END-(6-31) (2 and 5 nmol, icv), or with kappa-antagonists, Mr1452 MS and Mr2266 BS (10 mg/kg BW, ip), reversed electroshock-induced decrease in LH concentrations. beta-funaltrexamine (beta-FNA), an irreversible mu 1-opiate receptor antagonist, was partially effective in blocking the inhibitory effect of stress on LH levels. Neither passive immunization with anti-enkephalin nor the pretreatment with the delta-opiate receptor antagonist, ICI 154,129, (10 and 100 nmol, icv) modified the effect of stress. We then evaluated which endogenous opioid ligands and/or receptors might mediate the inhibitory effect on LH levels of 2 nmol ovine CRF injected icv. Anti-beta-END serum and beta-human END-(6-31), reversed the CRF-induced decrease of LH concentrations, whereas beta-FNA was only partially active. Anti-DYN-A and anti-ENK serum, kappa- and delta-antagonists did not prevent the decline of LH levels in rats receiving CRF centrally. These data suggest that stress-induced inhibition of LH secretion involves the stimulation of beta-END and DYN-A systems via mu/epsilon- or kappa-opiate receptors and that the decrease in circulating LH levels induced by centrally administered CRF may be mediated by the activation of beta-END system. Therefore, it is possible that the activation of the central CRF/beta-END pathway may play an important role in the stress-induced inhibition of reproductive functions.
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阿片诱导的纳洛酮对雄性大鼠血清黄体生成激素水平影响的增强：Mu 激动剂的特异性。
DOI：
--
发表时间：
1983
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Cicero,TJ;Owens,DP;Schmoeker,PF;Meyer,ER
通讯作者：
Meyer,ER
DOI：
--
发表时间：
1982-03
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
S. Ward;P. Portoghese;A. Takemori
通讯作者：
S. Ward;P. Portoghese;A. Takemori
影响因子：
4.1
作者：
SWANSON, LW;SAWCHENKO, PE;VALE, WW
通讯作者：
VALE, WW
影响因子：
56.9
作者：
RIVIER, C;RIVIER, J;VALE, W
通讯作者：
VALE, W
阿片类镇痛药增加兔脑脊液内源性阿片样活性的能力比较。
影响因子：
6.1
作者：
Kachur,JF;Rosemond,R;Welch,S;Bowman,ER;Martin,BR;Brase,DA;Dewey,WL
通讯作者：
Dewey,WL