Regional Difference in Sex Steroid Action on Formation of Morphological Sex Differences in the Anteroventral Periventricular Nucleus and Principal Nucleus of the Bed Nucleus of the Stria Terminalis

Kanaya, Moeko; Tsuda, Mumeko C.; Sagoshi, Shoko; Nagata, Kazuhiro; Morimoto, Chihiro; Thu, Chaw Kyi Tha; Toda, Katsumi; Kato, Shigeaki; Ogawa, Sonoko; Tsukahara, Shinji

doi:10.1371/journal.pone.0112616

Cited by 25 publications

(46 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the volume and neuron numbers of the AVPV in ERα knockout male mice become similar to those in female mice compared with wild-type male mice (Kanaya et al, 2014). In contrast, there is no significant effect of lacking the ERβ gene on the sexually dimorphic formation of the BNSTp and AVPV (Kanaya et al, 2014;Tsukahara et al, 2011). However, there are reports showing that administration of an ERβ agonist, as well as an ERα agonist, into postnatal females has a pharmacological effect to increase the number of BNSTp neurons in mice (Hisasue et al, 2010) and decrease the number of AVPV neurons in rats (Patchev et al, 2004).…”

Section: Contribution Of Sex Steroids To the Sexually Dimorphic Formamentioning

confidence: 81%

“…The volume and neuron numbers of the BNSTp in male mice are decreased by deletion of the ERα gene and become similar to those in female mice (Tsukahara et al, 2011). In addition, the volume and neuron numbers of the AVPV in ERα knockout male mice become similar to those in female mice compared with wild-type male mice (Kanaya et al, 2014). In contrast, there is no significant effect of lacking the ERβ gene on the sexually dimorphic formation of the BNSTp and AVPV (Kanaya et al, 2014;Tsukahara et al, 2011).…”

Section: Contribution Of Sex Steroids To the Sexually Dimorphic Formamentioning

confidence: 84%

See 1 more Smart Citation

Estrogenic regulation of social behavior and sexually dimorphic brain formation

Ogawa

Tsukahara

Choleris

et al. 2020

Neuroscience & Biobehavioral Reviews

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Contribution Of Sex Steroids To the Sexually Dimorphic Formamentioning

confidence: 81%

Section: Contribution Of Sex Steroids To the Sexually Dimorphic Formamentioning

confidence: 84%

Estrogenic regulation of social behavior and sexually dimorphic brain formation

Ogawa

Tsukahara

Choleris

et al. 2020

Neuroscience & Biobehavioral Reviews

Self Cite

View full text Add to dashboard Cite

show abstract

“…We demonstrate that CRFR1 cells at P0 co‐express ERα, while previous work has shown that the P0 AVPV/PeN is largely devoid of ERβ (Zuloaga, Zuloaga, Hinds, Carbone, & Handa, ). In addition, androgen receptor (AR) levels are barely detectable at P0 (Juntti et al, ; Kanaya et al, ). Apoptosis is potentially responsible for the observed sex difference in the AVPV as others have shown that perinatal androgen secretions trigger cell death in the developing AVPV (Forger et al, ; Kelly, Varnum, Krentzel, Krug, & Forger, ).…”

Section: Discussionmentioning

confidence: 99%

Characterization and gonadal hormone regulation of a sexually dimorphic corticotropin‐releasing factor receptor 1 cell group

Rosinger

Jacobskind

Bulanchuk

et al. 2018

J of Comparative Neurology

View full text Add to dashboard Cite

Corticotropin‐releasing factor binds with high affinity to CRF receptor 1 (CRFR1) and is implicated in stress‐related mood disorders such as anxiety and depression. Using a validated CRFR1‐green fluorescent protein (GFP) reporter mouse, our laboratory recently discovered a nucleus of CRFR1 expressing cells that is prominent in the female rostral anteroventral periventricular nucleus (AVPV/PeN), but largely absent in males. This sex difference is present in the early postnatal period and remains dimorphic into adulthood. The present investigation sought to characterize the chemical composition and gonadal hormone regulation of these sexually dimorphic CRFR1 cells using immunohistochemical procedures. We report that CRFR1‐GFP‐ir cells within the female AVPV/PeN are largely distinct from other dimorphic cell populations (kisspeptin, tyrosine hydroxylase). However, CRFR1‐GFP‐ir cells within the AVPV/PeN highly co‐express estrogen receptor alpha as well as glucocorticoid receptor. A single injection of testosterone propionate or estradiol benzoate on the day of birth completely eliminates the AVPV/PeN sex difference, whereas adult gonadectomy has no effect on CRFR1‐GFP cell number. These results indicate that the AVPV/PeN CRFR1 is regulated by perinatal but not adult gonadal hormones. Finally, female AVPV/PeN CRFR1‐GFP‐ir cells are activated following an acute 30‐min restraint stress, as assessed by co‐localization of CRFR1‐GFP cells with phosphorylated (p) CREB. CRFR1‐GFP/pCREB cells were largely absent in the male AVPV/PeN. Together, these data indicate a stress and gonadal hormone responsive nucleus that is unique to females and may contribute to sex‐specific stress responses.

show abstract

“…Thus, incomplete masculinization of the MeA may cause an improper functioning of the neural circuitry for the expression of male-type social behaviors. Testosterone and/or estradiol are involved in development of sexually dimorphic brain morphology by promoting cell proliferation, differentiation, or survival, or by inducing apoptosis in a sex-specific manner in certain brain regions (41)(42)(43)(44)(45). However, the exact mechanisms of ERα-mediated action of testosterone for full masculinization of the MeA structure and function during the pubertal period still remain unknown and need to be elucidated in future studies.…”

Section: Discussionmentioning

confidence: 99%

Pubertal activation of estrogen receptor α in the medial amygdala is essential for the full expression of male social behavior in mice

Sato

Nakata

Musatov

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Testosterone plays a central role in the facilitation of male-type social behaviors, such as sexual and aggressive behaviors, and the development of their neural bases in male mice. The action of testosterone via estrogen receptor (ER) α, after being aromatized to estradiol, has been suggested to be crucial for the full expression of these behaviors. We previously reported that silencing of ERα in adult male mice with the use of a virally mediated RNAi method in the medial preoptic area (MPOA) greatly reduced sexual behaviors without affecting aggressive behaviors whereas that in the medial amygdala (MeA) had no effect on either behavior. It is well accepted that testosterone stimulation during the pubertal period is necessary for the full expression of male-type social behaviors. However, it is still not known whether, and in which brain region, ERα is involved in this developmental effect of testosterone. In this study, we knocked down ERα in the MeA or MPOA in gonadally intact male mice at the age of 21 d and examined its effects on the sexual and aggressive behaviors later in adulthood. We found that the prepubertal knockdown of ERα in the MeA reduced both sexual and aggressive behaviors whereas that in the MPOA reduced only sexual, but not aggressive, behavior. Furthermore, the number of MeA neurons was reduced by prepubertal knockdown of ERα. These results indicate that ERα activation in the MeA during the pubertal period is crucial for male mice to fully express their male-type social behaviors in adulthood.T estosterone plays a central role in the regulation of male-type social behaviors in many mammalian species. It is known that testosterone facilitates the expression of sexual and aggressive behaviors through two kinds of actions. During the developmental period, testosterone exerts its "organizational action" to irreversibly masculinize the sexually undifferentiated brain and build the male-type neural network. In adulthood, testosterone exerts "activational action" to regulate the function of the fully masculinized neural network. As well as acting through androgen receptors (ARs), testosterone also acts through estrogen receptor (ER) α or ERβ, after being aromatized to estradiol (E2). Because the expression of sexual and aggressive behaviors is greatly reduced in aromatase knockout (ArKO) and ERα knockout (αERKO) male mice, aromatization of testosterone and its action via ERα have been suggested to be crucial for the facilitation of male-type social behaviors in mice (1-8). However, the exact timing and brain site(s) of ERα activation crucial for the expression of sexual and aggressive behaviors remain undetermined.In our previous study, we demonstrated site-specific involvement of ERα in the activational action of testosterone by using a virally mediated RNAi method. In this study, knocking down of ERα in the medial preoptic area (MPOA) of gonadally intact adult male mice suppressed sexual behavior while in the ventromedial nucleus (VMN) of hypothalamus reduced both sexual and aggressive behaviors...

show abstract

Regional Difference in Sex Steroid Action on Formation of Morphological Sex Differences in the Anteroventral Periventricular Nucleus and Principal Nucleus of the Bed Nucleus of the Stria Terminalis

Cited by 25 publications

References 43 publications

Estrogenic regulation of social behavior and sexually dimorphic brain formation

Estrogenic regulation of social behavior and sexually dimorphic brain formation

Characterization and gonadal hormone regulation of a sexually dimorphic corticotropin‐releasing factor receptor 1 cell group

Pubertal activation of estrogen receptor α in the medial amygdala is essential for the full expression of male social behavior in mice

Contact Info

Product

Resources

About