Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

Lima-Hernández, Francisco Javier; Beyer, Carlos; Gómora‐Arrati, Porfirio; García‐Juárez, Marcos; Encarnación-Sánchez, José L; Etgen, Anne M.; González‐Flores, Oscar

doi:10.1016/j.yhbeh.2012.09.004

Cited by 12 publications

(8 citation statements)

References 59 publications

(67 reference statements)

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“…Intracerebroventricular infusion of the MAPK PD98059 inhibitor decreased lordosis behaviour acutely induced by progestins, peptides, prostaglandin E 2 and by vagino‐cervical stimulation in oestrogen‐primed rats . Intracerebroventricular or intra‐VMH infusion of the Src kinase inhibitor PP2 also reduced lordosis behaviour induced by progestins and non steroidal agents . Notably, both ERs and PRs elicit rapid cellular responses independent of gene transcription by activating various signalling mechanisms, including the Src/MAPK pathway in human breast cancer T47D cell proliferation .…”

Section: Discussionmentioning

confidence: 99%

“…This general time course of drug effects was observed in previous studies that administered Rp‐cAMPS, KT5823, PP2 or KT5823 by the i.c.v. route or directly into the brain region of interest …”

Section: Discussionmentioning

confidence: 99%

“…An additional 1.5 minutes was allowed for drug diffusion before the removal of the infusion needle. E 2, EB, Rp‐cAMPS, KT5823, PD98059 and PP2 doses were obtained from previous work …”

Section: Methodsmentioning

confidence: 99%

“…Intracerebral administration of Rp‐cAMPS, an inhibitor of PKA, reduced lordosis behaviour induced by ring A‐reduced progestins, gonadotrophin‐releasing hormone, prostaglandin E 2, leptin, and vaginocervical stimulation in E 2 ‐primed rats . Intracerebral administration of KT5823 (PKG inhibitor), PP2 (Src kinase inhibitor) or PD98059 (MAPK inhibitor) also reduced lordosis induced by progestins and a variety of other agents, suggesting the PKG and Src/MAPK pathways are also implicated in the display of female sexual behaviour in OVX, oestrogen‐primed rats.…”

Section: Introductionmentioning

confidence: 99%

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Protein kinase inhibitors infused intraventricularly or into the ventromedial hypothalamus block short latency facilitation of lordosis by oestradiol

Domínguez-Ordoñez

García‐Juárez

Lima-Hernández

et al. 2019

J Neuroendocrinology

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| INTRODUC TI ONIn ovariectomised (OVX) rats, lordosis behaviour can be induced by repeated or high doses of oestradiol (E 2 ) without subsequent treatment with progesterone. 1-8 Moreover, intracerebral or subcutaneous administration of E 2 induces lordosis behaviour with a short latency in E 2 -benzoate (EB) primed rats. 9-12 Despite the great variety of physiological and reproductive effects of oestrogens, the cellular Abstract An injection of unesterified oestradiol (E 2 ) facilitates receptive behaviour in E 2 benzoate (EB)-primed, ovariectomised female rats when it is administered i.c.v. or systemically. The present study tested the hypothesis that inhibitors of protein kinase A (PKA), protein kinase G (PKG) or the Src/mitogen-activated protein kinase (MAPK) complex interfere with E 2 facilitation of receptive behaviour. In Experiment 1, lordosis induced by i.c.v. infusion of E 2 was significantly reduced by i.c.v. administration of Rp-cAMPS, a PKA inhibitor, KT5823, a PKG inhibitor, and PP2 and PD98059, Src and MAPK inhibitors, respectively, between 30 and 240 minutes after infusion. In Experiment 2, we determined whether the ventromedial hypothalamus (VMH) is one of the neural sites at which those intracellular pathways participate in lordosis behaviour induced by E 2 . Administration of each of the four protein kinase inhibitors into the VMH blocked facilitation of lordosis induced by infusion of E 2 also into the VMH.These data support the hypothesis that activation of several protein kinase pathways is involved in the facilitation of lordosis by E 2 in EB-primed rats.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…An additional 1.5 minutes was allowed for drug diffusion before the removal of the infusion needle. E 2, EB, Rp‐cAMPS, KT5823, PD98059 and PP2 doses were obtained from previous work …”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protein kinase inhibitors infused intraventricularly or into the ventromedial hypothalamus block short latency facilitation of lordosis by oestradiol

Domínguez-Ordoñez

García‐Juárez

Lima-Hernández

et al. 2019

J Neuroendocrinology

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“…Progesterone receptors A and B are found in the plasma membrane, although it is unlikely that progesterone receptor‐D1 receptor transactivation occurs because D1 and progesterone receptors A and B do not co‐immunoprecipitate . It is likely that the D1 and progesterone receptor signalling pathways act within a given lordosis neurocircuit, potentially through progesterone receptor directly interacting through the Src kinase pathway within the cytoplasm .…”

Section: Steroid Activation Of Sexual Receptivitymentioning

confidence: 99%

Temporal and Concentration‐Dependent Effects of Oestradiol on Neural Pathways Mediating Sexual Receptivity

Micevych

Sinchak

2013

J Neuroendocrinology

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The acceptance of estradiol signaling through receptors found in the cell membrane, as well as, the nucleus has provided for a re-examination of timing and location of estradiol actions on neural circuits mediating sexual receptivity (lordosis). Estradiol membrane signaling involves the transactivation of metabotropic glutamate receptors (mGluR) that transduce steroid information through PKC signaling cascades producing rapid activation of lordosis regulating circuits. It has been known for some time that estradiol initially produces an inhibition of the medial preoptic nucleus (MPN). We have demonstrated that underlying this inhibition is estradiol acting in the arcuate nucleus to induce β-endorphin release which inhibits the MPN through a μ-opioid receptor mechanism. This transient inhibition is relieved by either subsequent progesterone treatment or longer exposure to higher doses of estradiol to facilitate lordosis behavior. We review recent findings about estradiol membrane signaling inducing dendritic spine formation in the arcuate nucleus that is critical for estradiol induction of sexual receptivity. Moreover, we discuss the evidence that in addition to ERα, several other putative membrane estrogen receptors facilitate lordosis behavior through regulation of the arcuate nucleus. These include the GRP30 and the STX activated Gq-mER. Finally, we report on the importance of GABA acting at GABAB receptors for estradiol membrane signaling that regulates lordosis circuit activation and sexual receptivity.

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Female Sexual Behavior

Pfaus

Jones

Flanagan‐Cato³

et al. 2015

Knobil and Neill's Physiology of Reproduction

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Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

Cited by 12 publications

References 59 publications

Protein kinase inhibitors infused intraventricularly or into the ventromedial hypothalamus block short latency facilitation of lordosis by oestradiol

Protein kinase inhibitors infused intraventricularly or into the ventromedial hypothalamus block short latency facilitation of lordosis by oestradiol

Temporal and Concentration‐Dependent Effects of Oestradiol on Neural Pathways Mediating Sexual Receptivity

Female Sexual Behavior

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