Cellular and molecular mechanisms of action of ovarian steroid hormones. II: Regulation of sexual behavior in female rodents
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F25%3A43921394" target="_blank" >RIV/00023752:_____/25:43921394 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11240/25:10492123
Výsledek na webu
<a href="https://www.sciencedirect.com/science/article/pii/S0149763424004159?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0149763424004159?via%3Dihub</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.neubiorev.2024.105946" target="_blank" >10.1016/j.neubiorev.2024.105946</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Cellular and molecular mechanisms of action of ovarian steroid hormones. II: Regulation of sexual behavior in female rodents
Popis výsledku v původním jazyce
Female sexual behaviors in rodents (lordosis and appetitive or “proceptive” behaviors) are induced through a genomic mechanism by the sequential actions of estradiol (E2) and progesterone (P), or E2 and testosterone (T) at their respective receptors. However, non-steroidal agents, such as gonadotropin-releasing hormone (GnRH), Prostaglandin E2 (PGE2), noradrenaline, dopamine, oxytocin, α-melanocyte stimulating hormone, nitric oxide, leptin, apelin, and others, facilitate different aspects of female sexual behavior through their cellular and intracellular effects at the membrane and genomic levels in ovariectomized rats primed with E2. These neurotransmitters often act as intermediaries of E2 and P (or T). The classical model of steroid hormone action through intracellular receptor binding has been complemented by an alternative scenario wherein the steroid functions as a transcription factor after binding the receptor protein to DNA. Another possible mechanism occurs through the activation of second messenger systems (cyclic AMP, cyclic GMP, calcium), which subsequently initiate phosphorylation events via diverse kinase systems (protein kinases A, G, or C). These kinases target the progesterone receptor (PR) or associated effector proteins that connect the PR to the trans-activation machinery. This may also happen to the androgen receptor (AR). In addition, other cellular mechanisms could be involved since the chemical structure of these non-steroidal agents causes a change in their lipophobicity that prevents them from penetrating the cell and exerting direct transcriptional effects; however, they can exert effects on different components of the cell membrane activating a cross-talk between the cell membrane and the regulation of the transcriptional mechanisms.
Název v anglickém jazyce
Cellular and molecular mechanisms of action of ovarian steroid hormones. II: Regulation of sexual behavior in female rodents
Popis výsledku anglicky
Female sexual behaviors in rodents (lordosis and appetitive or “proceptive” behaviors) are induced through a genomic mechanism by the sequential actions of estradiol (E2) and progesterone (P), or E2 and testosterone (T) at their respective receptors. However, non-steroidal agents, such as gonadotropin-releasing hormone (GnRH), Prostaglandin E2 (PGE2), noradrenaline, dopamine, oxytocin, α-melanocyte stimulating hormone, nitric oxide, leptin, apelin, and others, facilitate different aspects of female sexual behavior through their cellular and intracellular effects at the membrane and genomic levels in ovariectomized rats primed with E2. These neurotransmitters often act as intermediaries of E2 and P (or T). The classical model of steroid hormone action through intracellular receptor binding has been complemented by an alternative scenario wherein the steroid functions as a transcription factor after binding the receptor protein to DNA. Another possible mechanism occurs through the activation of second messenger systems (cyclic AMP, cyclic GMP, calcium), which subsequently initiate phosphorylation events via diverse kinase systems (protein kinases A, G, or C). These kinases target the progesterone receptor (PR) or associated effector proteins that connect the PR to the trans-activation machinery. This may also happen to the androgen receptor (AR). In addition, other cellular mechanisms could be involved since the chemical structure of these non-steroidal agents causes a change in their lipophobicity that prevents them from penetrating the cell and exerting direct transcriptional effects; however, they can exert effects on different components of the cell membrane activating a cross-talk between the cell membrane and the regulation of the transcriptional mechanisms.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30103 - Neurosciences (including psychophysiology)
Návaznosti výsledku
Projekt
—
Návaznosti
V - Vyzkumna aktivita podporovana z jinych verejnych zdroju
Ostatní
Rok uplatnění
2025
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Neuroscience and Biobehavioral Reviews
ISSN
0149-7634
e-ISSN
1873-7528
Svazek periodika
168
Číslo periodika v rámci svazku
"Article number: 105946"
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
31
Strana od-do
1-31
Kód UT WoS článku
001367988200001
EID výsledku v databázi Scopus
2-s2.0-85210000827