Identification of a seven transmembrane helix receptor for corticotropin-releasing factor and sauvagine in mammalian brain

Chang, Chia-Ping; Pearse, Richard V.; O’Connell, Shawn M.; Rosenfeld, Michael G.

doi:10.1016/0896-6273(93)90230-o

Cited by 520 publications

(290 citation statements)

References 53 publications

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“…An antisense probe was designed, based on the published sequence of the cloned rat-CRH receptor [4,14]. The probe targeted the spliced region between the third and fourth transmembrane domains [4], and consisted of a 35 oligodeoxynucleotide encompassing bases 211-246 of the CRH-receptor cDNA, which is entirely within the 'spliced' region.…”

Section: Generation and Labeling Of Oligodeoxynucleotide Probesmentioning

confidence: 99%

“…Binding studies may also provide limited information on the actual site of receptor synthesis because ligands may bind to neural receptors on cell bodies and along dendrites and axons [17]. The recent cloning of cDNAs encoding the rat CRH receptor [4,14] permits mapping the distribution of cells expressing CRH receptor messenger ribonucleic acid (mRNA) [17,21]. In this study, we report on the developmental profile of CRH receptor mRNA in limbic brain regions of the rat brain.…”

Section: Introductionmentioning

confidence: 99%

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Developmental profile of messenger RNA for the corticotropin-releasing hormone receptor in the rat limbic system

Avishai-Eliner

Baram

1996

Developmental Brain Research

101

110

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The ontogeny of corticotropin-releasing hormone (CRH) receptor messenger ribonucleic acid (mRNA) in rat brain, using in situ hybridization, is the focus of this study. The developmental profile of CRH receptor using binding assays and receptor autoradiography has been reported, but may be confounded by the presence of a binding protein. The recent cloning of the rat CRH receptor gene has permitted the use of in situ hybridization histochemistry to map the distribution of cells expressing CRH receptor mRNA in the developing brain. We used antisense 35 S-labeled oligodeoxynucleotide probes for the two reported splice-variants of the CRH receptor mRNA, which yielded essentially identical localization patterns. CRH receptor mRNA was clearly detectable in infant brain starting on the second postnatal day. Signal in hippocampal CA1, CA2 and CA3a increased to 300-600% of adult levels by postnatal day 6 with a subsequent gradual decline. In the amygdala, in contrast, CRH receptor mRNA abundance increased steadily between the second and the ninth postnatal days, to levels twice higher than those in the adult. In the cortex, CRH receptor mRNA levels were high on postnatal day 2 and decreased to adult levels by day 12. Transient signal over the hypothalamic paraventricular nucleus, observed on the second postnatal day, was not evident at older ages. These results demonstrate robust synthesis of CRH receptor as early as on the second postnatal day and unique region-specific developmental profiles for CRH receptor gene expression.

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Section: Generation and Labeling Of Oligodeoxynucleotide Probesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Developmental profile of messenger RNA for the corticotropin-releasing hormone receptor in the rat limbic system

Avishai-Eliner

Baram

1996

Developmental Brain Research

101

110

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“…Both CRF and Ucn1 contribute to stress responses via G protein-coupled receptors [29,58,62]. The CRF type 1 receptor (CRF 1 receptor) [6,11,65], for which both CRF and Ucn1 have high affinity [62], is predominately expressed in the brain and pituitary gland.…”

Section: Introductionmentioning

confidence: 99%

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

et al. 2013

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Corticotropin-releasing factor (CRF) activates the pituitary-adrenal axis during stress, and shows anorectic effects via CRF type 1 receptors in the hypothalamus.Both urocortin (Ucn) 2 and Ucn3 also act as anorectic neuropeptides via CRF type 2 receptors. Leptin, a product of the obesity gene secreted mainly from adipose tissue, reduces food intake and increases energy expenditure. A possible interaction between leptin and CRF/Ucns has been suggested, as leptin can regulate expression and activation of CRF and Ucns in the hypothalamus. This study aimed to explore the possible function of leptin in the hypothalamus, and its effects in regulating CRF and Ucns. The study identified mRNA expression of the leptin receptor (Ob-R) and its subtypes, CRF, and Ucn2/3 in mouse hypothalamic N39 cells. Leptin stimulated signal transducer and activators of transcription type 3 (STAT3) phosphorylation, directly increased the mRNA levels of both CRF and Ucn2/3 in hypothalamic cells, and increased Ob-Rb mRNA levels. A Janus kinase inhibitor inhibited the leptin-mediated increase in STAT3 phosphorylation, and then the increases in CRF and Ucn2/3 mRNA levels. Leptin may contribute to a stress response or anorectic effect via the regulation 2 of CRF and Ucn2/3 in the hypothalamus.

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“…CRH exerts pleiotropic e ects, mediated by two di erent, adenylate cyclase-coupled, receptors, the CRH receptor types 1 and 2 (CRH-R1 and CRH-R2) (Chang et al, 1993;Perrin et al, 1993;. CRH-R1 and CRH-R2 have been shown to produce di erent e ects in the same murine behavioural model (Radulovic et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Divergent effects of corticotropin releasing hormone on endothelial cell nitric oxide synthase are associated with different expression of CRH type 1 and 2 receptors

Cantarella

Lempereur

Lombardo

et al. 2001

British J Pharmacology

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1 Endothelium is a target for an array of factors involved in in¯ammation. Endothelial cells express receptors for CRH, a neuropeptide produced during in¯ammation. We report both the concentration-dependent inhibitory e ect of CRH upon cytokine-stimulated nitrite release by H5V murine endothelioma cells, and its stimulatory one in HUVEC cells. 2 Western blot analysis showed that CRH inhibits cytokine-stimulated iNOS protein in H5V cells, and, instead, potentiated it in HUVEC cells. 3 H5V cells expressed both CRH receptors (CRH-R1 and R2) mRNAs, whereas HUVEC cells expressed the CRH-R2 mRNA solely. 4 CRH increased medium nitrites and iNOS protein expression in H5V cells pretreated with the selective CRH-R1 antagonist CP 154,526. However, the selective CRH-R2 antagonist anti-Svg-30 failed to produce similar e ects. In fact, anti-Svg-30 inhibited CRH-induced increase of nitrite release and iNOS expression in HUVEC cells. 5 Our results con®rm the activating role of CRH on endothelial cells, although it suggests its possible inhibitory role in the late phase of the in¯ammatory response. NO-mediated e ects of CRH on endothelial cells could be exploited in therapeutic strategies related to in¯ammatory and/or degenerative diseases.

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Identification of a seven transmembrane helix receptor for corticotropin-releasing factor and sauvagine in mammalian brain

Cited by 520 publications

References 53 publications

Developmental profile of messenger RNA for the corticotropin-releasing hormone receptor in the rat limbic system

Developmental profile of messenger RNA for the corticotropin-releasing hormone receptor in the rat limbic system

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

Divergent effects of corticotropin releasing hormone on endothelial cell nitric oxide synthase are associated with different expression of CRH type 1 and 2 receptors

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