Testosterone levels in plasma and testes of neonatal mice

Motelica-Heino, Ion; Castanier, M; Corbier, P.; Edwards, David A.; Roffi, J

doi:10.1016/0022-4731(88)90351-2

Cited by 73 publications

(46 citation statements)

References 12 publications

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“…In mice, there are two well established periods of androgen exposure experienced by perinatal males: one occurs during the last few days of gestation and another on PND1 (Pang and Tang, 1984;Motelica-Heino et al, 1988;Corbier et al, 1992). Gestational androgen secretion appears to be intact in GPR54 KO males, as indicated by the presence of male genitalia and accessory sex organs, along with male-like anogenital distance on PND1 (which are all androgen dependent).…”

Section: Discussionmentioning

confidence: 99%

The Kisspeptin Receptor GPR54 Is Required for Sexual Differentiation of the Brain and Behavior

Kauffman¹,

Park²,

et al. 2007

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GPR54 is a G-protein-coupled receptor, which binds kisspeptins and is widely expressed throughout the brain. Kisspeptin-GPR54 signaling has been implicated in the regulation of pubertal and adulthood gonadotropin-releasing hormone (GnRH) secretion, and mutations or deletions of GPR54 cause hypogonadotropic hypogonadism in humans and mice. Other reproductive roles for kisspeptin-GPR54 signaling, including the regulation of developmental GnRH secretion or sexual behavior in adults, have not yet been explored. Using adult wild-type (WT) and GPR54 knock-out (KO) mice, we first tested whether kisspeptin-GPR54 signaling is necessary for male and female sexual behaviors. We found that hormone-replaced gonadectomized GPR54 KO males and females displayed appropriate gender-specific adult sexual behaviors. Next, we examined whether GPR54 signaling is required for proper display of olfactory-mediated partner preference behavior. Testosterone-treated WT males preferred stimulus females rather than males, whereas similarly treated WT females and GPR54 KO males showed no preference for either sex. Because olfactory preference is sexually dimorphic and organized during development by androgens, we assessed whether GPR54 signaling is essential for sexual differentiation of other sexually dimorphic traits. Interestingly, adult testosterone-treated GPR54 KO males displayed "female-like" numbers of tyrosine hydroxylaseimmunoreactive and Kiss1 mRNA-containing neurons in the anteroventral periventricular nucleus and likewise possessed fewer motoneurons in the spino-bulbocavernosus nucleus than did WT males. Our findings indicate that kisspeptin-GPR54 signaling is not required for male or female copulatory behavior, provided there is appropriate adulthood hormone replacement. However, GPR54 is necessary for proper male-like development of several sexually dimorphic traits, likely by regulating GnRH-mediated androgen secretion during "critical windows" in perinatal development.

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Section: Discussionmentioning

confidence: 99%

The Kisspeptin Receptor GPR54 Is Required for Sexual Differentiation of the Brain and Behavior

Kauffman¹,

Park²,

et al. 2007

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“…Prenatal flutamide likely rescues tg males from death by binding to ARs and blocking the effects of endogenous T [32][33][34] . However, blocking androgen action prenatally does not prevent expression of the disease later in life because flutamide-rescued tg males exhibit the same motor deficits in adulthood as untreated tg males.…”

Section: Discussionmentioning

confidence: 99%

Prenatal Flutamide Enhances Survival in a Myogenic Mouse Model of Spinal Bulbar Muscular Atrophy

et al. 2010

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Background: Spinal bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene, and mutant AR is presumed to act in motoneurons to cause SBMA. However, we found that mice overexpressing wild-type (wt) AR solely in skeletal muscle fibers display the same androgen-dependent disease phenotype as when mutant AR is broadly expressed, challenging the assumptions that only an expanded AR can induce disease and that SBMA is strictly neurogenic. We have previously reported that AR toxicity was ligand dependent in our model, and that very few transgenic (tg) males survived beyond birth. Methods: We tested whether the AR antagonist flutamide could block perinatal toxicity. tg males were treated prenatally with flutamide and assessed for survival and motor behavior in adulthood. Results: Prenatal treatment with flutamide rescued tg male pups from perinatal death, and, as adults, such perinatally rescued tg males showed an SBMA phenotype that was comparable to that of previously described untreated tg males. Moreover, tg males carrying a mutant endogenous allele for AR – the testicular feminization mutation (tfm) – and thus having functional AR only in muscle fibers nevertheless displayed the same androgen-dependent disease phenotype as adults. Conclusions: These mice represent an excellent model to study the myogenic contribution to SBMA as they display many of the core features of disease as other mouse models. These data demonstrate that AR acting exclusively in muscle fibers is sufficient to induce SBMA symptoms and that flutamide is protective perinatally.

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“…In newborn mice, pTc reaches a peak about 2 h after birth, then decreases till 6 h after delivery, leading to the hypothesis that this peak might initiate developmental processes differentiating mechanisms involved in adult intermale attack (Motelica-Heino et al, 1988). Castration is more efficient when it occurs within the first hour after birth: at adulthood, no mouse showed any fighting behavior before receiving androgens (MotelicaHeino et al, 1993).…”

Section: Steroid Action On Olfactory Acuity Gabaergic Activity and mentioning

confidence: 97%

“…The hypothesis of an early sensitization of the areas of the brain involved in adult offense behavior such as the olfactory bulbs has been put forward (Motelica-Heino et aL, 1988). Hormones produced early during development have permanent effects which are reversible.…”

Section: Steroid Action On Olfactory Acuity Gabaergic Activity and mentioning

confidence: 99%

Olfaction, GABAergic neurotransmission in the olfactory bulb, and intermale aggression in mice: Modulation by steroids

Guillot

Chapouthier

1996

Behav Genet

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A model to explain individual differences in mice for the propensity to attack male conspecifics is proposed. In the first part of the paper, the relation between olfaction and intermale aggression is discussed emphasizing the importance of olfactory cues provided by the opponent and their subsequent processing by the attacking male. The physiological role of GABA in the olfactory pathway is presented in the second part of the paper. The third part investigates the possible modulating action of steroids on the GABA-A receptor complex, intermale aggression, and olfaction. We hypothesize that at least part of the individual differences in the propensity to attack may be explained by a differential olfactory recognition and discrimination of the opponent as a stranger through a differential processing threshold of the olfactory cues provided by the urine of the opponent. A possible modulation of this threshold by steroids, especially testosterone, is also discussed.

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Testosterone levels in plasma and testes of neonatal mice

Cited by 73 publications

References 12 publications

The Kisspeptin Receptor GPR54 Is Required for Sexual Differentiation of the Brain and Behavior

The Kisspeptin Receptor GPR54 Is Required for Sexual Differentiation of the Brain and Behavior

Prenatal Flutamide Enhances Survival in a Myogenic Mouse Model of Spinal Bulbar Muscular Atrophy

Olfaction, GABAergic neurotransmission in the olfactory bulb, and intermale aggression in mice: Modulation by steroids

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