Activation by Serotonin and Noradrenaline of Vasopressin and Oxytocin Expression in the Mouse Paraventricular and Supraoptic Nuclei

Vacher, Claire-Marie; Fretier, Philippe; Créminon, Christophe; Calas, A.; Hardin‐Pouzet, Hélène

doi:10.1523/jneurosci.22-05-01513.2002

Cited by 110 publications

(98 citation statements)

References 59 publications

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“…Intracerebroventricular administration of TRH leads to increased concentrations of oxytocin and vasopressin in the hypothalamus and in the posterior pituitary in nursing rats (62). Noradrenalin and serotonin are known to control arginine-vasopressin and oxytocin secretion in the systemic circulation, and have recently been shown to do the same in the PVN and the SON in mouse (63). However, TRH had no effect on noradrenalin release from neurons of the PVN (64).…”

Section: Discussionmentioning

confidence: 95%

Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

Fjeldheim¹,

Høvring²,

Løseth³

et al. 2005

eur j endocrinol

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Background: The accepted function of the hypothalamic peptide, thyrotrophin-releasing hormone (TRH), is to initiate release of thyrotrophin (TSH) from the pituitary. A physiological role for TRH in lactating rats has not yet been established. Methods: Tissues were prepared from random-cycling and lactating rats and analysed using Northern blot, real time RT-PCR and quantitative in situ hybridisation.Results: This study demonstrates that TRH receptor 1 (TRHR1) mRNA expression is up-regulated in the pituitary and in discrete nuclei of the hypothalamus in lactating rats, while proTRH mRNA expression levels are increased only in the hypothalamus. The results were corroborated by quantitative in situ analysis of proTRH and TRHR1. Bromocriptine, which reduced prolactin (PRL) concentrations in plasma of lactating and nursing rats, also counteracted the suckling-induced increase in TRHR1 mRNA expression in the hypothalamus, but had an opposite effect in the pituitary. These changes were confined to the hypothalamus and the amygdala in the brain.Conclusions: The present study shows that the mechanisms of suckling-induced lactation involve region-specific regulation of TRHR1 and proTRH mRNAs in the central nervous system notably at the hypothalamic level. The results demonstrate that continued suckling is critical to maintain plasma prolactin (PRL) levels as well as proTRH and TRHR1 mRNA expression in the hypothalamus. Increased plasma PRL levels may have a positive modulatory role on the proTRH/TRHR1 system during suckling.

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Section: Discussionmentioning

confidence: 95%

Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

Fjeldheim¹,

Høvring²,

Løseth³

et al. 2005

eur j endocrinol

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“…In addition to the effects on dopamine receptors previously mentioned, the serotonin and norepinephrine systems have also been shown to increase oxytocin mRNA transcription in both the supraoptic and paraventricular nucleus, though the mechanism of these interactions has not been fully elucidated (Jorgensen et al, 2003;Vacher et al, 2002). Chronic cocaine administration through its multiple effects on these systems could result in alterations in neurotransmitter receptor levels and an overall change in the sensitivity of these systems.…”

Section: Discussionmentioning

confidence: 99%

Impact of gestational cocaine treatment or prenatal cocaine exposure on early postpartum oxytocin mRNA levels and receptor binding in the rat

et al. 2008

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Prior research reported decreased oxytocin levels in specific brain regions correlated with disruptions in maternal care following gestational cocaine treatment in rats. Similarly, prenatal exposure to cocaine impaired subsequent maternal behavior in adulthood, but behavioral alterations were not associated with decreases in oxytocin levels in the same brain regions as were found in their cocainetreated rat dams. To determine if other aspects of the oxytocin system are disrupted by cocaine treatment or prenatal exposure to cocaine during critical time points associated with maternal care, oxytocin mRNA transcription and receptor binding were examined on postpartum day two in relevant brain regions following gestational treatment with, or prenatal exposure to, either cocaine or saline. We hypothesized that oxytocin mRNA levels and receptor binding would be differentially affected by cocaine in the early postpartum period of dams and their offspring. Our findings indicate that gestational cocaine treatment resulted in significant increases in oxytocin mRNA levels in only the paraventricular nucleus of cocaine-treated dams, with almost significant increases in both generations in the supraoptic nucleus, but no significant effects of cocaine on receptor binding in either generation of dams. These findings indicate that in addition to oxytocin levels, cocaine treatment or prenatal exposure primarily affects oxytocin mRNA synthesis, with little effect on receptor binding in specific brain regions associated with maternal behavior in the early postpartum period of the rat.

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“…Brain fixation and sectioning were performed as described previously (Vacher et al 2002). Coronal brain sections (50 mm) were cut on a vibroslicer (1000Plus, Harvard Apparatus, Holliston, MA, USA) and blocked for endogenous peroxidase in 1% H 2 O 2 .…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…Coronal brain sections (50 mm) were cut on a vibroslicer (1000Plus, Harvard Apparatus, Holliston, MA, USA) and blocked for endogenous peroxidase in 1% H 2 O 2 . Sections were incubated for 24 h at 4 8C with mouse anti-PRL-R (1:200; Affinity BioReagents, Golden, CO, USA) or rabbit anti-ObRb prepared in our laboratory, and revelations performed as described previously (Vacher et al 2002). Control experiments were performed by omitting the primary antibodies.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Lack of cross-desensitization between leptin and prolactin signaling pathways despite the induction of suppressor of cytokine signaling 3 and PTP-1B

Roy¹,

Benomar²,

Bailleux³

et al. 2007

Journal of Endocrinology

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Hyperprolactinemia and hyperleptinemia occur during gestation and lactation with marked hyperphagia associated with leptin resistance. Prolactin (PRL) induces the expression of orexigenic neuropeptide Y (NPY) through the activation of JAK-2/STAT-3 signaling pathway in hypothalamic paraventricular nucleus (PVN) leading to hyperphagia. PRL may also act through the inhibition of anorexigenic effect of leptin via induction of suppressor of cytokine signaling 3 (SOCS-3). This paper aimed to co-localize PRL (PRL-R) and leptin (ObRb) receptors in the hypothalamus of female rats and investigate the possible cross-desensitization between PRL-R and ObRb. We showed that: 1) PRL-R and ObRb are expressed in the PVN and co-localized in the same neurons; 2) in lactating females leptin failed to activate JAK-2/STAT-3 signaling pathway; 3) in Chinese Hamster Ovary (CHO) stably co-expressing PRL-R and ObRb, overexposure to PRL did not affect leptin signaling but totally abolished PRL-dependent STAT-5 phosphorylation. The overexposure to leptin produces similar results with strong alteration of leptin-dependent STAT-3 phosphorylation, whereas PRL-dependent STAT-5 was not affected; and 4) CHO-ObRb/PRL-R cells overexposure to leptin or PRL induces the expression of negative regulators SOCS-3 and PTP-1B. Thus, we conclude that these negative regulators affect specifically the inducer signaling pathway; for instance, SOCS-3 induced by PRL will affect PRL-R signaling but not ObRb signaling and vice versa. Finally, the lack of cross-desensitization between PRL-R and ObRb suggests that hyperphagia observed during gestation and lactation may be attributed to a direct effect of PRL on NPYexpression, and is most likely exacerbated by the physiological leptin resistance state.

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Activation by Serotonin and Noradrenaline of Vasopressin and Oxytocin Expression in the Mouse Paraventricular and Supraoptic Nuclei

Cited by 110 publications

References 59 publications

Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

Impact of gestational cocaine treatment or prenatal cocaine exposure on early postpartum oxytocin mRNA levels and receptor binding in the rat

Lack of cross-desensitization between leptin and prolactin signaling pathways despite the induction of suppressor of cytokine signaling 3 and PTP-1B

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