Ontogenesis of κ-opioid receptors in rat brain using [3H]U-69593 as a binding ligand

Kitchen, Ian; Kelly, Mary; Viveros, María-Paz

doi:10.1016/0014-2999(90)90157-2

Cited by 29 publications

(16 citation statements)

References 9 publications

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“…A number of studies also showed that opioid receptor blockade with naloxone reverted the change in sexual behavior observed in the PS group [41, 44, 45]. Endogenous opioidergic systems have been shown to play pivotal roles in the regulation of neural development [15, 20]. The study described here shows that naloxone treatment (1 mg/kg) performed 30 min before prenatal stress reverted macrophage activity damage presented by male and female offspring on PND30.…”

Section: Discussionsupporting

confidence: 52%

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Fonseca

Sakai²,

Carvalho-Freitas³

et al. 2005

Neuroendocrinology

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The present study analyzed the effects of maternal stress (PS) and/or naloxone treatment on the activity of peritoneal macrophage in male and female Swiss mice offspring. Pregnant female rats received a daily footshock (0.2 mA) and/or a naloxone injection from gestational day 15 to 19. Experiments were performed on postnatal day 30 on male and female pups. The following results were obtained in male offspring: (1) PS decreased both the index and the percentage of phagocytosis, this decrement being reversed by naloxone treatment, and (2) naloxone alone decreased the percentage of phagocytosis. The following results were obtained in female offspring: (1) PS decreased spontaneous and phorbol myristate acetate-induced macrophage oxidative burst, this decrement being reversed by naloxone pretreatment, and (2) PS decreased both the index and percentage of the phagocytosis, this effect was prevented by naloxone treatment. These data are discussed focussing on a putative neuroimmune interaction involving opioidergic systems during the ontogeny of the central nervous and immune systems.

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Section: Discussionsupporting

confidence: 52%

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Fonseca

Sakai²,

Carvalho-Freitas³

et al. 2005

Neuroendocrinology

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“…These experiments were performed as described previously (Kitchen et al, 1990;Slowe et al, 1999). Animals were killed by decapitation, and brains were removed and immediately immersed in isopentane maintained at Ϫ35°C on dry ice.…”

Section: Autoradiographic Experimentsmentioning

confidence: 99%

Sex Difference in κ-Opioid Receptor (KOPR)-Mediated Behaviors, Brain Region KOPR Level and KOPR-Mediated Guanosine 5′-O-(3-[35S]Thiotriphosphate) Binding in the Guinea Pig

Wang

Rasakham²,

Huang³

et al. 2011

The Journal of Pharmacology and Experimental Therapeutics

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We examined whether sex differences in -opioid receptor (KOPR) pharmacology exist in guinea pigs, which are more similar to humans in the expression level and distribution of KOPR in the brain than rats and mice. The KOPR agonist trans-(Ϯ)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl)benzeneacetamide methanesulfonate (U50,488H) produced a dose-dependent increase in abnormal postures and immobility with more effects in males than females. Males also showed more U50,488H-induced antinociception in the paw pressure test than females. Pretreatment with the KOPR antagonist norbinaltorphimine blocked U50,488H-induced abnormal body postures and antinociception. In contrast, inhibition of cocaine-induced hyperambulation by U50,488H was more effective in females than males. Thus, sex differences in the effects of U50,488H are endpoint-dependent. We then examined whether sex differences in KOPR levels and KOPR-mediated G protein activation in brain regions may contribute to the observed differences using quantitative in vitro autora-

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“…The activation of these opioid receptors also increases phospholipase C activity and causes a transient increase in the activation of the mitogen-activated protein kinase (MAPK), 1 ERK1, and ERK2-2 (9 -11). The expression of opioid receptors has been examined primarily by in situ hybridization, immunohistochemistry, and ligand binding assays (12)(13)(14)(15).…”

mentioning

confidence: 99%

Induction of the Mouse κ-Opioid Receptor Gene by Retinoic Acid in P19 Cells

Park

Loh

et al. 2002

Journal of Biological Chemistry

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Opioid receptors are located throughout the central and peripheral nervous systems and interact with opiate drugs such as morphine to affect the perception of pain, consciousness, and autonomic function. Three types of opioid receptors, , ␦, and , have been defined and cloned (1, 2). These receptors belong to the superfamily of G-protein-coupled receptors and regulate a number of signaling pathways (3-8). The regulated pathways include the inhibition of adenylyl cyclase activity and N-type and L-type Ca 2ϩ channels and the activation of inwardly rectifying K ϩ channels. The activation of these opioid receptors also increases phospholipase C activity and causes a transient increase in the activation of the mitogen-activated protein kinase (MAPK), 1 ERK1, and ERK2-2 (9 -11). The expression of opioid receptors has been examined primarily by in situ hybridization, immunohistochemistry, and ligand binding assays (12-15).The mouse -opioid receptor (KOR) gene has been isolated in several laboratories (16). The genetic basis underlying the ontogenesis of KOR gene has been revealed in transgenic animal models in our laboratory (17). The mouse gene contains four exons and utilizes two promoters. A total of three KOR mRNA isoforms designated as a, b, and c can be generated (18). We have previously reported the activities of dual promoters of mouse KOR gene in the P19 cell line (19). Recently, we have demonstrated the up-regulation of the endogenous KOR mRNA by depleting vitamin A in developing animals and the downregulation of KOR mRNA in differentiating P19 cells treated with retinoic acid (RA) for 2 days or longer. This is mediated by a negative regulatory element, which contains an Ikaros binding site within intron I (promoter II) of the KOR gene (20, 21).Interestingly, a short term (within 24 h) treatment with RA induces KOR expression in P19. We now report the mechanism mediating the early inducing effect of RA on KOR gene expression in P19 cells. We first identified a cis-acting element containing a putative Sp1 binding site (GC box) in the promoter I of the mouse KOR gene. We then demonstrated that Sp1 could bind to this GC box, and the hypophosphorylation of Sp1 enhanced its DNA binding affinity to this element. The inhibition of ERKs pathway enhanced RA induction of this promoter activity, whereas the phosphatase inhibitor suppressed RA induction of this promoter. These results demonstrated that RA-induced KOR gene expression could be mediated by the enhanced binding of Sp1 to this promoter, a consequence of hypophosphorylation of Sp1 by blocking the ERK pathway. EXPERIMENTAL PROCEDURESPlasmid Constructs-Luciferase fusion plasmids were constructed by inserting various upstream regulatory sequences into a promoterless and enhancerless luciferase vector pGL3B (Promega, Madison, WI). The K45 and K19 plasmids were constructed as described previously (21). K45 contains a KOR-genomic fragment of 1320 bp from the BamHI site to the ATG codon. K19 was a truncation of K45 that contains a 904-bp KOR-genomic fragment from Bam...

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Ontogenesis of κ-opioid receptors in rat brain using [3H]U-69593 as a binding ligand

Cited by 29 publications

References 9 publications

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Sex Difference in κ-Opioid Receptor (KOPR)-Mediated Behaviors, Brain Region KOPR Level and KOPR-Mediated Guanosine 5′-O-(3-[35S]Thiotriphosphate) Binding in the Guinea Pig

Induction of the Mouse κ-Opioid Receptor Gene by Retinoic Acid in P19 Cells

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