Activation of μ-Opioid Receptors Inhibits Lordosis Behavior in Estrogen and Progesterone-Primed Female Rats

Acosta-Martínez, Maricedes; Etgen, Anne M.

doi:10.1006/hbeh.2001.1741

Cited by 59 publications

(31 citation statements)

References 42 publications

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“…The MPN is an important node in the neurocircuitry that regulates sexual receptivity (Acosta-Martinez and Etgen, 2002; Pfaus and Pfaff, 1992; Powers, 1972; Sinchak et al, 2007; Sinchak and Micevych, 2001; Sinchak et al, 2004; Sirinathsinghji, 1984; Torii et al, 1996, 1999). In this model circuit, EB initiates signaling via binding to a membrane-associated ERα (mERα) that complexes with, and transactivates metabotropic glutamate receptor-1a (mGluR1a; Dewing et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Tamoxifen and ICI 182,780 activate hypothalamic G protein-coupled estrogen receptor 1 to rapidly facilitate lordosis in female rats

Long

Mana

et al. 2017

Hormones and Behavior

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In the female rat, sexual receptivity (lordosis) can be facilitated by sequential activation of estrogen receptor (ER) α and G protein-coupled estrogen receptor 1 (GPER) by estradiol. In the estradiol benzoate (EB) primed ovariectomized (OVX) rat, EB initially binds to ERα in the plasma membrane that complexes with and transactivates metabotropic glutamate receptor 1a to activate β-endorphin neurons in the arcuate nucleus of the hypothalamus (ARH) that project to the medial preoptic nucleus (MPN). This activates MPN μ-opioid receptors (MOP), inhibiting lordosis. Infusion of non-esterified 17β-estradiol into the ARH rapidly reduces MPN MOP activation and facilitates lordosis via GPER. Tamoxifen (TAM) and ICI 182,780 (ICI) are selective estrogen receptor modulators that activate GPER. Therefore, we tested the hypothesis that TAM and ICI rapidly facilitate lordosis via activation of GPER in the ARH. Our first experiment demonstrated that injection of TAM intraperitoneal, or ICI into the lateral ventricle, deactivated MPN MOP and facilitated lordosis in EB-primed rats. We then tested whether TAM and ICI were acting rapidly through a GPER dependent pathway in the ARH. In EB-primed rats, ARH infusion of either TAM or ICI facilitated lordosis and reduced MPN MOP activation within 30 minutes compared to controls. These effects were blocked by pretreatment with the GPER antagonist, G15. Our findings demonstrate that TAM and ICI deactivate MPN MOP and facilitate lordosis in a GPER dependent manner. Thus, TAM and ICI may activate GPER in the CNS to produce estrogenic actions in neural circuits that modulate physiology and behavior.

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Section: Introductionmentioning

confidence: 99%

Tamoxifen and ICI 182,780 activate hypothalamic G protein-coupled estrogen receptor 1 to rapidly facilitate lordosis in female rats

Long

Mana

et al. 2017

Hormones and Behavior

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“…Specificity among opioid receptors, as well as neuroanatomical site specificity, is observed in this course of action. [51][52][53][54] The indirect route of action of this multiplicative set of gene inductions is likely to allow the female to participate in sex behavior sequences.…”

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confidence: 99%

Hormonal symphony: steroid orchestration of gene modules for sociosexual behaviors

Mong

Pfaff

2004

Mol Psychiatry

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Genes induced by estrogens in the mammalian forebrain influence a variety of neural functions. Among them, reproductive behavior mechanisms are very well understood. Their functional genomics provide a theoretical paradigm for linking genes to neural circuits to behavior. We propose that estrogen-induced genes are organized in modules: Growth of hypothalamic neurons; Amplification of the estrogen effect by progesterone; Preparative behaviors; Permissive actions on sex behavior circuitry; and Synchronization of mating behavior with ovulation. These modules may represent mechanistic routes for CNS management of successful reproduction. Moreover, new microarray results add estrogen-dependent genes, including some expressed in glia, suggesting possible hormone-dependent neuronal/ glial coordination. Molecular Psychiatry (2004) 9, 550-556. doi:10.1038/sj.mp.4001493Keywords: sex; estrogen; gene; hypothalamus; lordosis; arousal; noradrenalin; acetylcholine; oxytocin; enkephalin; opioid; GnRH; LHRH; neurotrophic; anxiety Sexual behaviors are important for psychiatry. Not only hypersexual disorders but also concerns about lack of sexual desire are prominent, internationally, in the psychiatric landscape. Further, in some traditions of psychiatric theory, sexual problems are held to be at the root of apparently unrelated syndromes. Finally, biological thought has held that sexual affiliations provide the bauplan, the structural precedent, for a wide variety of other social relations, both normal or abnormal. Fortunately, the molecular analysis of stereotyped sexual behaviors has benefited greatly from several strategic advantages: Even in mammals, simple stimuli and responses permit neural net analysis. Steroid hormones acting through nuclear receptors which are transcription factors invoke regulated gene expression, for example, in hypothalamic neurons.1 In turn, these neurons control mating behavior circuits.Drawing hormone-regulated gene expression into the explanation of mammalian sex behavior has proceeded rapidly. Here we theoretically propose a gene network-really, a micronet-downstream of estrogen action in the forebrain responsible for courtship and lordosis behavior in females. Not a massive review of the literature or an original data report, this paper comprises an attempt to draw different transcriptional systems into a new theoretical formulation. These efforts to explain hormone-driven behaviors have benefited from Rosenfeld's example of genetic network control over pituitary gland development.2 Both direct and indirect causal routes are depicted below.Causal routes, downstream from genomic action; a modular system emergent The primary sex behavior of female quadrupeds, lordosis, depends on defined physical signals: cutaneous stimuli and estrogens þ progestins 1 (E þ P). The neural circuit has been worked out; estrogen-dependent transcription in ventromedial hypothalamic cells allows permissive signals to the midbrain central gray, thus enabling the rest of the circuit. In the absence of fear or anxiety-pro...

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“…β-END is one of the posttranslational products released by proopiomelanocortin (POMC) neurons and an endogenous ligand for μ-opioid receptors (MOP). MPN MOP activation inhibits lordosis in maximally receptive females (Acosta-Martinez & Etgen, 2002;Pfaus & Pfaff, 1992;Sinchak & Micevych, 2001;Sirinathsinghji, 1986). The MOP, being a G proteincoupled receptor, are internalized rapidly into early endosomes upon activation by endogenous ligands (Arden, Segredo, Wang, Lameh, & Sadaee, 1995;Keith et al, 1998, 1996Mantyh et al, 1995Mestek et al, 1995;Sharma, Klee, & Nirenberg, 1977;von Zastrow, Keith, Zaki, & Evans, 1994).…”

Section: Reproductive Behaviormentioning

confidence: 97%

Orphanin FQ-ORL-1 Regulation of Reproduction and Reproductive Behavior in the Female

2015

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Activation of μ-Opioid Receptors Inhibits Lordosis Behavior in Estrogen and Progesterone-Primed Female Rats

Cited by 59 publications

References 42 publications

Tamoxifen and ICI 182,780 activate hypothalamic G protein-coupled estrogen receptor 1 to rapidly facilitate lordosis in female rats

Tamoxifen and ICI 182,780 activate hypothalamic G protein-coupled estrogen receptor 1 to rapidly facilitate lordosis in female rats

Hormonal symphony: steroid orchestration of gene modules for sociosexual behaviors

Orphanin FQ-ORL-1 Regulation of Reproduction and Reproductive Behavior in the Female

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