Premium
Protein kinase inhibitors infused intraventricularly or into the ventromedial hypothalamus block short latency facilitation of lordosis by oestradiol
Author(s) -
DomínguezOrdóñez Raymundo,
GarcíaJuárez Marcos,
LimaHernández Francisco J.,
GómoraArrati Porfirio,
DomínguezSalazar Emilio,
LunaHernández Ailyn,
Hoffman Kurt L.,
Blaustein Jeffrey D.,
Etgen Anne M.,
GonzálezFlores Oscar
Publication year - 2019
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12809
Subject(s) - lordosis , lordosis behavior , endocrinology , protein kinase a , medicine , facilitation , protein kinase c , chemistry , estradiol benzoate , hypothalamus , cgmp dependent protein kinase , kinase , mapk/erk pathway , ventromedial nucleus of the hypothalamus , hormone , ovariectomized rat , biology , mitogen activated protein kinase kinase , neuroscience , biochemistry , radiography , radiology
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.