Regulation by oestrogens of tachykinin NK3 receptor expression in the rat uterus

Pinto, Francisco M.; Magraner, Josefina; Ausina, Pilar; Anselmi, Elsa; Martı́n, Julio D.; Candenas, Luz

doi:10.1016/s0014-2999(97)00150-7

Cited by 16 publications

(17 citation statements)

References 12 publications

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“…Nerve terminals are associated with the myometrial and vascular smooth muscle and are distributed throughout the endocervix [19,[23][24][25]. Tachykinins have a direct contractile effect in uterine smooth muscle from different species, including humans [20][21][22][24][25][26][27][28][29][30][31][32]. The three tachykinin receptors are expressed in the rat uterus, and their expression and function are selectively and differentially regulated by ovarian steroids [22,[30][31][32].…”

Section: Introductionmentioning

confidence: 99%

A Role for Tachykinins in Female Mouse and Rat Reproductive Function1

Pintado

Pinto

Pennefather

et al. 2003

Biology of Reproduction

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Tachykinins may be involved in reproduction. A reverse transcription-polymerase chain reaction assay was used to analyze the expression of tachykinins and tachykinin receptors in different types of reproductive cells from mice. The preprotachykinin (PPT) genes, PPT-A, PPT-B and PPT-C, that encode substance P/neurokinin A, neurokinin B, and hemokinin-1, respectively, and the genes that encode the tachykinin NK1, NK2, and NK3 receptors were all expressed, at different levels, in the uterus of superovulated, unfertilized mice. The mRNA of neprilysin (NEP), the main enzyme involved in tachykinin metabolism, was also expressed in the uterus. Isolated cumulus granulosa cells expressed PPT-A, PPT-B, PPT-C, and NEP and low levels of the tachykinin NK1 and NK2 receptors. Mouse oocytes expressed PPT-A and -B mRNA transcripts. A low expression of the three tachykinin receptors was observed but PPT-C and NEP were undetectable. Two- and 8- to 16-cell mouse embryos expressed only a low-abundance transcript corresponding to the NK1 receptor. However, the mRNAs of PPT-B, PPT-C and NEP appeared in blastocyst-stage embryos. A low-abundance transcript corresponding to the NK2 receptor was the only target gene detected in mice sperm. Female mice or rats treated neonatally with capsaicin showed a reduced fertility. A reduction in litter size was observed in female rats treated in vivo with the tachykinin NK3 receptor antagonist SR 142801. These data show that tachykinins of both neuronal and nonneuronal origin are differentially expressed in various types of reproductive cells and may play a role in female reproductive function.

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Section: Introductionmentioning

confidence: 99%

A Role for Tachykinins in Female Mouse and Rat Reproductive Function1

Pintado

Pinto

Pennefather

et al. 2003

Biology of Reproduction

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“…Results of our earlier studies also suggest that NK2-R activation causes strong uterine contractions in both the estrogen-dominated and non-estrogen-dominated rat uterus [16] and that activation of both NK1-Rs and NK3-Rs plays a significant role in mediating sensory neuropeptide control of uterine contractility. This hypothesis is supported by the identification of expression of NK1-R, NK2-R, and NK3-R mRNA in the rat uterus [10][11][12]. Perhaps of greater significance is the accumulating evidence suggesting that uterine contractility mediated particularly through the NK3-R may be regulated by estrogen.…”

Section: Discussionmentioning

confidence: 94%

“…Perhaps of greater significance is the accumulating evidence suggesting that uterine contractility mediated particularly through the NK3-R may be regulated by estrogen. Investigators of NK3-R mRNA expression in the rat uterus have reported a dramatic reduction in NK3-R mRNA levels in the estrogen-dominated uterus [10,12]. Results of functional studies also suggest that NK3-R-mediated uterine contractility is downregulated by estrogen [10,12,16].…”

Section: Discussionmentioning

confidence: 99%

“…Expression of NK-Rs in the rat uterus has been investigated by reverse transcription polymerase chain reaction (RT-PCR) amplification of specific NK-R mRNAs [10][11][12] and by demonstration of uterine contractility in response to selective NK-R agonists [11][12][13][14][15][16]. These studies suggest that all three NK-Rs are expressed in the rat uterus.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, we observed that in non-estrogen-dominated uterine tissue activation of the NK3-R resulted in a sustained uterotonic response, whereas in estrogen-dominated tissue a monophasic contraction was elicited upon NK3-R activation. Other researchers investigating the expression of NK-Rs by RT-PCR have suggested that NK3-R is particularly strongly regulated by estrogen [10,12].…”

Section: Introductionmentioning

confidence: 99%

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Estrogen-Dependent Regulation of Neurokinin 3 Receptor-Mediated Uterine Contractility in the Rat1

Crane

Williams

Nimmo

et al. 2002

Biology of Reproduction

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The receptors for neurokinin 1 (NK1-R), neurokinin 2 (NK2-R), and neurokinin 3 (NK3-R) are expressed and functionally active in the uterus, promoting strong contractions of the myometrium. Previously, we demonstrated that myometrial contractility activated by the NK-Rs is regulated by estrogen. In the current study, we furthered our investigations of the role of estrogen in the regulation of NK3-R-mediated myometrial contractility. Estrogen promotes both heterologous and homologous desensitization of NK3-R-mediated uterine contractility. In tissue obtained from estrogen-dominated rats (ovariectomized estrogen-treated rats and rats in estrus), the magnitude of uterine contractions decreased in response to consecutive additions of the NK3-R-selective agonist senktide. By addition of the fourth dose of agonist, the contractile response was routinely barely above baseline. In contrast, in tissue obtained from non-estrogen-dominated rats consecutive doses of senktide resulted in contractions of identical magnitude. The homologous desensitization was specific to the NK3-R, and the desensitization of the NK3-R-mediated response did not affect the magnitude or nature of uterine contractions in response to NK1-R or NK2-R activation. Furthermore, heterologous and homologous desensitization of NK3-R-mediated contractility is dependent upon the duration of exposure to estrogen. This complex mechanism appears to be important in intact tissue; capsaicin-mediated release of endogenous neuropeptides resulted in a desensitization of response to subsequent stimulation with senktide in estrogen-dominated uterine tissue.

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