Inhibition by N-methyl-d-aspartic acid (NMDA) receptor antagonist of lordosis behavior induced by estrogen followed by progesterone or luteinizing hormone-releasing hormone (LHRH) in the rat

Gargiulo, Pascual Ángel; Muñoz, Virginia Andía; Donoso, Alfredo O.

doi:10.1016/0031-9384(92)90407-s

Cited by 18 publications

(15 citation statements)

References 15 publications

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“…Although this may be a likely scenario for LHRH secretion, it is not likely in the current behavioral model. A number of studies have now shown that inhibition of the NMDA receptor with their respective antagonists would block the P-and LHRH-facilitated lordosis behavior (17,(63)(64)(65)(66). In the lordosis model, if LHRH-(1-5) acts as an antagonist to the NMDA receptor, then it should not facilitate lordosis unless it blocks an upstream site from the LHRH-(1-5) action.…”

Section: Discussionmentioning

confidence: 97%

Facilitation of Lordosis in Rats by a Metabolite of Luteinizing Hormone Releasing Hormone

Wu¹,

Glucksman²,

Roberts³

et al. 2006

Endocrinology

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In the female rat, ovulation is preceded by a marked increase in the release of the decapeptide, LHRH, culminating in a preovulatory LH surge, which coincides with a period of sexual receptivity. The decapeptide, LHRH, is processed by a zinc metalloendopeptidase EC 3.4.24.15 (EP24.15) that cleaves the hormone at the Tyr(5)-Gly(6) bond. We have previously reported that the autoregulation of LHRH gene expression can also be mediated by its metabolite, LHRH-(1-5). Given the central function of LHRH in reproduction and reproductive behavior, we examined the role of the metabolite, LHRH-(1-5), in mediation of LHRH-facilitated reproductive behavior. Intracerebroventricular administration of LHRH-(1-5) facilitated sexual behavior responses, similar to those facilitated by the decapeptide LHRH, in ovariectomized estradiol-primed female rats. Furthermore, immunoneutralization of EP24.15 resulted in the inhibition of the LHRH-facilitated lordosis but had no inhibitory effects on LHRH-(1-5)-facilitated lordosis. The LHRH antagonist, Antide, was capable of inhibiting LHRH-facilitated lordosis, without affecting LHRH-(1-5)-facilitated lordosis. Collectively, these results suggest a role for LHRH metabolites in the facilitation of female receptive behavior in rats.

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Section: Discussionmentioning

confidence: 97%

Facilitation of Lordosis in Rats by a Metabolite of Luteinizing Hormone Releasing Hormone

Wu¹,

Glucksman²,

Roberts³

et al. 2006

Endocrinology

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“…Dopamine administration inhibits facilitation of lordosis by GnRH in the VTA (Sirinathsinghji et aL, 1986). Excitatory amino acids, on the other hand, play a stimulatory role in GnRH-induced mating behavior, however, their particular site of action remains unknown (Gargiulo et aL, 1992;Hsu et aL, 1993). Finally, mating itself is reported to activate more than one-half of the GnRH neurons in the MPOA, and this response appears to be augmented by exposure to estrogen and progesterone (Pfaus et al, 1994).…”

Section: Female Reproductive Behaviormentioning

confidence: 93%

Hormonal and neurotransmitter regulation of GnRH gene expression and related reproductive behaviors

et al. 1996

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Gonadotropin-releasing hormone (GnRH), having a highly conserved structure across mammalian species, plays a pivotal role in the control of the neuroendocrine events and the inherent sexual behaviors essential for reproductive function. Recent advances in molecular genetic technology have contributed greatly to the investigation of several aspects of GnRH physiology, particularly steroid hormone and neurotransmitter regulation of GnRH gene expression. Behavioral studies have focused on the actions of GnRH in steroid-sensitive brain regions to understand better its role in the facilitation of mating behavior. To date, however, there are no published reports which directly correlate GnRH gene expression and reproductive behavior. The intent of this article is to review the current understanding of the way in which changes in GnRH gene expression, and modifications of GnRH neuronal activity, may ultimately influence reproductive behavior.

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“…The stimulatory effect of NMDA on lordosis behavior also required an estrogen background as no effect was observed in non-estrogen-primed ovariectomized rats. Along these lines, administration of the NMDA receptor antagonists, AP-5 or MK-801, significantly inhibited lordosis behavior in estrogen plus progesterone-treated ovariectomized rats (192). It should be pointed out that there is not total agreement in the literature concerning glutamate regulation of lordosis behavior, as there have been a few reports suggesting that glutamate inhibits lordosis behavior (190,191).…”

Section: B Eaas and Reproductive Behaviormentioning

confidence: 99%

“…Systemic administration of NMDA has also been reported to induce lordosis behavior in estrogen-primed ovariectomized rats (137). In contrast, treatment with a non-NMDA receptor antagonist had no effect on lordosis behavior (192). It is not clear why the various studies disagree; however, glutamate receptor antagonist studies appear to support a stimulatory role of glutamate in reproductive behavior.…”

Section: B Eaas and Reproductive Behaviormentioning

confidence: 99%

Excitatory Amino Acids: Evidence for a Role in the Control of Reproduction and Anterior Pituitary Hormone Secretion*

Brann

Mahesh

1997

Endocrine Reviews

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Inhibition by N-methyl-d-aspartic acid (NMDA) receptor antagonist of lordosis behavior induced by estrogen followed by progesterone or luteinizing hormone-releasing hormone (LHRH) in the rat

Cited by 18 publications

References 15 publications

Facilitation of Lordosis in Rats by a Metabolite of Luteinizing Hormone Releasing Hormone

Facilitation of Lordosis in Rats by a Metabolite of Luteinizing Hormone Releasing Hormone

Hormonal and neurotransmitter regulation of GnRH gene expression and related reproductive behaviors

Excitatory Amino Acids: Evidence for a Role in the Control of Reproduction and Anterior Pituitary Hormone Secretion*

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