FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1987685637> ?p ?o ?g. }

• W1987685637 endingPage "485" @default.
• W1987685637 startingPage "473" @default.
• W1987685637 abstract "Cholecystokinin, substance P and methionine enkephalin all regulate the display of reproductive behaviour. Their expression is exquisitely regulated by estrogen in the limbic–hypothalamic circuit, a circuit that regulates the display of estrogen-sensitive female reproductive behaviour. Relatively little is known, however, about the interaction of endogenous opioid peptides with cholecystokinin and substance P in the limbic–hypothalamic circuit. Opiates antagonize the release of cholecystokinin and substance P in the hypothalamus and periaqueductal gray and stimulate cholecystokinin messenger RNA levels in the amygdala. To determine the effect of endogenous opioid input on estrogen-induced cholecystokinin, enkephalin and substance P expression, in situ hybridization histochemistry was used to examine estrogen-induced messenger RNA levels of these neuropeptides in specific nuclei of the limbic system and hypothalamus in the presence of opiate receptor antagonists. Estrogen treatment of ovariectomized rats significantly elevated cholecystokinin messenger RNA levels in the central portion of the medial preoptic nucleus, the encapsulated portion of the bed nucleus of the stria terminalis and the posterodorsal medial amygdala, as well as increased preproenkephalin and preprotachykinin messenger RNA levels in the ventromedial hypothalamic nucleus and the posterodorsal medial amygdala. The universal opiate receptor antagonist naltrexone and the δ-opiate receptor antagonist naltrindole each potentiated the estrogen-induced increase and elevated cholecystokinin messenger RNA levels an additional 1.9- to 2.8-fold depending on the nucleus examined, but had no effect on the estrogen-induced expression of either preproenkephalin or preprotachykinin messenger RNA. β-Funaltrexamine, a μ-opiate receptor antagonist, had no effect on the medial preoptic or medial amygdaloid cholecystokinin messenger RNA levels or on the estrogen-induced expression of preproenkephalin messenger RNA but did cause a decrease in estrogen-induced cholecystokinin messenger RNA levels in the bed nucleus of the stria terminalis and a decrease in the preprotachykinin messenger RNA levels in the ventromedial hypothalamic nucleus. These results indicate that endogenous opioids, acting on the δ-opiate receptor within nuclei of the limbic–hypothalamic circuit, restrain the estrogen-induced increase of cholecystokinin messenger RNA expression. Activation of the μ-opiate receptor, however, may facilitate cholecystokinin messenger RNA expression in the bed nucleus of the stria terminalis and preprotachykinin messenger RNA expression in the ventromedial hypothalamic nucleus. Thus, endogenous opioid peptides may act in a site- and receptor-specific manner to modulate estrogen-induced neuropeptide levels in the limbic system and hypothalamus." @default.
• W1987685637 created "2016-06-24" @default.
• W1987685637 creator A5017308765 @default.
• W1987685637 creator A5029348051 @default.
• W1987685637 date "1997-07-01" @default.
• W1987685637 modified "2023-09-27" @default.
• W1987685637 title "Opiate receptors modulate estrogen-induced cholecystokinin and tachykinin but not enkephalin messenger RNA levels in the limbic system and hypothalamus" @default.
• W1987685637 cites W1527057398 @default.
• W1987685637 cites W1528872814 @default.
• W1987685637 cites W1551555282 @default.
• W1987685637 cites W1598665107 @default.
• W1987685637 cites W160555191 @default.
• W1987685637 cites W1634437520 @default.
• W1987685637 cites W1969553615 @default.
• W1987685637 cites W1969653468 @default.
• W1987685637 cites W1969850608 @default.
• W1987685637 cites W1970270230 @default.
• W1987685637 cites W1970954584 @default.
• W1987685637 cites W1975158285 @default.
• W1987685637 cites W1978481532 @default.
• W1987685637 cites W1980435560 @default.
• W1987685637 cites W1981204355 @default.
• W1987685637 cites W1986411498 @default.
• W1987685637 cites W1988090037 @default.
• W1987685637 cites W1989425791 @default.
• W1987685637 cites W1990744299 @default.
• W1987685637 cites W1998131288 @default.
• W1987685637 cites W2005548493 @default.
• W1987685637 cites W2011645297 @default.
• W1987685637 cites W2013017751 @default.
• W1987685637 cites W2014287820 @default.
• W1987685637 cites W2016263894 @default.
• W1987685637 cites W2022709379 @default.
• W1987685637 cites W2026519029 @default.
• W1987685637 cites W2027197361 @default.
• W1987685637 cites W2027998184 @default.
• W1987685637 cites W2029418812 @default.
• W1987685637 cites W2032363880 @default.
• W1987685637 cites W2033293623 @default.
• W1987685637 cites W2034534031 @default.
• W1987685637 cites W2034694607 @default.
• W1987685637 cites W2037175122 @default.
• W1987685637 cites W2038182479 @default.
• W1987685637 cites W2039065287 @default.
• W1987685637 cites W2044126244 @default.
• W1987685637 cites W2045722822 @default.
• W1987685637 cites W2049406563 @default.
• W1987685637 cites W2050633159 @default.
• W1987685637 cites W2050948990 @default.
• W1987685637 cites W2053311238 @default.
• W1987685637 cites W2062174284 @default.
• W1987685637 cites W2062919524 @default.
• W1987685637 cites W2068046521 @default.
• W1987685637 cites W2068911013 @default.
• W1987685637 cites W2070370133 @default.
• W1987685637 cites W2074369462 @default.
• W1987685637 cites W2076897614 @default.
• W1987685637 cites W2077261915 @default.
• W1987685637 cites W2083006866 @default.
• W1987685637 cites W2083491176 @default.
• W1987685637 cites W2085750612 @default.
• W1987685637 cites W2088431185 @default.
• W1987685637 cites W2091105506 @default.
• W1987685637 cites W2091807568 @default.
• W1987685637 cites W2093053031 @default.
• W1987685637 cites W2093088022 @default.
• W1987685637 cites W2122416811 @default.
• W1987685637 cites W2122744483 @default.
• W1987685637 cites W2133029605 @default.
• W1987685637 cites W2141857561 @default.
• W1987685637 cites W2142692419 @default.
• W1987685637 cites W2154072252 @default.
• W1987685637 cites W2160218663 @default.
• W1987685637 cites W2160284775 @default.
• W1987685637 cites W2429945967 @default.
• W1987685637 cites W4301036066 @default.
• W1987685637 doi "https://doi.org/10.1016/s0306-4522(97)00072-9" @default.
• W1987685637 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9284350" @default.
• W1987685637 hasPublicationYear "1997" @default.
• W1987685637 type Work @default.
• W1987685637 sameAs 1987685637 @default.
• W1987685637 citedByCount "23" @default.
• W1987685637 countsByYear W19876856372013 @default.
• W1987685637 countsByYear W19876856372015 @default.
• W1987685637 countsByYear W19876856372017 @default.
• W1987685637 countsByYear W19876856372022 @default.
• W1987685637 crossrefType "journal-article" @default.
• W1987685637 hasAuthorship W1987685637A5017308765 @default.
• W1987685637 hasAuthorship W1987685637A5029348051 @default.
• W1987685637 hasConcept C118303440 @default.
• W1987685637 hasConcept C126322002 @default.
• W1987685637 hasConcept C134018914 @default.
• W1987685637 hasConcept C170493617 @default.
• W1987685637 hasConcept C185592680 @default.
• W1987685637 hasConcept C2777003273 @default.
• W1987685637 hasConcept C2777593968 @default.
• W1987685637 hasConcept C2777803847 @default.
• W1987685637 hasConcept C2778140631 @default.

• next