Elsevier

Neuroscience Letters

Volume 212, Issue 1, 5 July 1996, Pages 68-70
Neuroscience Letters

Influence of opioid peptides on the priming action of estrogen on lordosis in ovariectomized rats

https://doi.org/10.1016/0304-3940(96)12763-4Get rights and content

Abstract

Lordosis in response to male mounting in estrogen-progesterone primed ovariectomized rats was facilitated by β-endorphin or metenkephalin but inhibited by leu-enkephalin if the peptides were injected into third ventricle at the time of estrogen-priming. It is suggested that opiodergic systems modulate the activation of the estrogen-dependent brain functions that control lordosis.

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      Such analyses revealed that the initial action of estradiol, in terms of lordosis, is to engage an inhibitory circuit that involved MPN-projecting β-END neurons [84,86]. Transient opioid inhibition action is needed for maximal sexual receptivity, but sustained activation of μ-opioid receptors (MOR) in the MPN inhibits sexual receptivity [59,84,91,92]. Subsequent steroid and pharmacological treatments that reduce estradiol-induced MOR activation facilitate lordosis [9,47,48,60,63,93].

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      If the initial actions of estradiol are blocked by treating with a selective estrogen receptor modulator (SERM), tamoxifen (TAM), then sexual receptivity is not facilitated (Etgen and Shamamian, 1986). Likewise, if opioid activity in the region of the MPN is blocked at the time of estradiol priming, then subsequent facilitation of sexual receptivity does not occur (Torii et al., 1995, 1996, 1997, 1999). Finally, in our model system, if the initial mERα-mGluR1a signaling that rapidly activates MPN MOP is blocked by mGluR1a antagonists, the animals are nonreceptive (Dewing et al., 2007).

    • Modulation of the arcuate nucleus-medial preoptic nucleus lordosis regulating circuit: A role for GABA<inf>B</inf> receptors

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      Inhibition of GABAB receptors in the ARH prior to estradiol treatment blocked the estradiol-induced MPN MOR activation and did not enhance sexual receptivity. This transient MOR-mediated inhibition is necessary for lordosis behavior, as initially demonstrated by Torii and colleagues (Torii and Kubo, 1994; Torii et al., 1995, 1996, 1999) who gave naloxone (a classical opioid receptor antagonist) prior to estradiol priming. We confirmed the importance of MOR by examining lordosis in a MOR knockout mouse in which full sexual receptivity could not be achieved compared to the wildtype controls (Sinchak et al., 2005).

    • Estradiol signaling in the regulation of reproduction and energy balance

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      Progesterone treatment must be delayed about 24 h after estradiol priming to facilitate lordosis (Sinchak and Micevych, 2001) to allow for the expression of progesterone receptors through the “priming” actions of estradiol through direct genomic actions of ERα, ERβ (Alves et al., 2000; Shughrue et al., 1997) and possibly through mER interactions that ultimately modulate transcription. For example, blocking classical opioid receptors with naloxone at the time of estradiol injection decreases the ability of progesterone 48 h later to facilitate lordosis (Torii and Kubo, 1994; Torii et al., 1995, 1996, 1999). The activation of μ-opioid receptors in the medial preoptic nucleus are driven by estradiol binding mERα that complex and transactivate mGluR1a mERα-mGluR1a actions in the ARH (Eckersell et al., 1998) indicating the potential for an alternative indirect mechanism for estradiol to induce progesterone receptor expression that is initiated through mERα.

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    We thank Prof. Dr. Y. Hiji (Department of Physiology, Faculty of Medicine, Tottori University, Japan) for valuable comments and critical reading of the manuscript.

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