Female sexual behavior in male rats: Effect of hour of castration at birth

Corbier, P.; Roffi, J; Rhoda, J.

doi:10.1016/0031-9384(83)90229-9

Cited by 57 publications

(24 citation statements)

References 15 publications

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“…A surge in circulating testosterone is evident during the period of E16-18 in the rat (Weisz and Ward, 1980). Furthermore, in the male rat, a dramatic increase in serum testosterone occurs during the first four hours of postnatal life (Dohler and Wuttke, 1974;Corbier et al, 1983).…”

Section: Circulating Androgen Levels Increase Transiently During Devementioning

confidence: 93%

Living or dying in three quarter time: Neonatal orchestration of hippocampal cell death pathways by androgens and excitatory GABA

Foradori¹

2008

Experimental Neurology

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In the immature brain, GABA (γ-aminobutyric acid) is an excitatory neurotransmitter. With development, GABA becomes inhibitory due to the changes in the expression level of chloride transporters, leading to a negative shift in chloride ions. Clinical evidence and studies in animal models indicate greater brain damage in male versus female neonates following a variety of neuronal insults. The recent finding of Nunez and McCarthy suggest a mechanism whereby androgens may endanger male neurons to the possible excitotoxic effects of excitatory GABA in neonates. Given our growing understanding of the excitatory immature GABAergic system and how sex, age and hormone milieu can influence this system, such studies might pave a path for novel clinical treatments to alleviate neonatal risk for brain injury.

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Section: Circulating Androgen Levels Increase Transiently During Devementioning

confidence: 93%

Living or dying in three quarter time: Neonatal orchestration of hippocampal cell death pathways by androgens and excitatory GABA

Foradori¹

2008

Experimental Neurology

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“…Much of our own work points to the importance of the first several hours after birth insofar as defeminization effects are concerned [5][6][7], It is probably particularly important that in the neonatal male rat, se rum and hypothalamic testosterone rise against a background of sharply falling se rum and hypothalamic progesterone. Resko [17] and Dorfman [8] have suggested that progesterone may protect against some of the organizing effects of androgens on cen tral nervous system tissue.…”

Section: Resultsmentioning

confidence: 99%

“…The increase in serum testosterone is paralleled by an in crease in hypothalamic testosterone and es tradiol, with the latter presumably derived from the conversion of testosterone to estra diol in hypothalamic tissue [18]. Increases in serum testosterone and hypothalamic testos terone and estradiol are not seen in females or males castrated at birth [18], and the fact that such males are completely feminized with respect to positive feedback and femi nine sexual behavior [5,6] is consonant with the notion that gonadal hormonal stimula tion during the first several hours after birth promotes defeminization.…”

Section: Introductionmentioning

confidence: 99%

“…Adult male rats show little or no positive gonado tropin feedback to injection of estradiol [ 15] and do not show feminine sexual behavior as adults [5,6]. In this sense, males can be said to be defeminized, and defeminization de pends upon the presence of testicular hor mones during the perinatal period [6], Whether it is testosterone or a metabolite of testosterone which actually effects the pre sumed neural changes critical for defemini zation remains an open question, but there is convincing evidence that the conversion of testosterone to 17(3-estradiol is an essential step in the process [14].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Progesterone on the Testosterone and Estradiol Levels in the Hypothalamus of Neonatal Rats

et al. 1987

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Pregnant female rats were injected with progesterone or oil from 18.5 up to 21.5 days of gestation. Rat pups were delivered by caesarian section, and pups delivered from progesterone-treated mothers were injected with 100 μg of progesterone and pups from oil-treated mothers were injected with oil. Two hours after delivery, pups were killed and hypothalamic testosterone and estradiol were determined by RIA. Control males had substantially higher concentrations of testosterone and estradiol in hypothalamus than control females. Treatment with progesterone did not affect the accumulation of testosterone in the hypothalamic tissue of neonatal males, but completely prevented the formation of estradiol in hypothalamic tissue. This result suggests that progesterone can inhibit hypothalamic aromatase activity in the neonate and may explain why progesterone can protect against some of the neural defeminizing effects of neonatally administered androgens.

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“…Males that are castrated within 3 h after birth show an increased sensi tivity to estrogen as adults. These animals display more receptive behavior than control males [168][169][170][171] and are more sensitive to sCCK-8 infusions than are intact males [25], Females treated with a single dose of testosterone propionate do not show a reduced sensitivity to estradiol benzoate, but are much less sensitive to the inhibitory effects of sCCK-8 infusions. These neonatally androge nized females show lordosis behavior after either of two doses of estradiol benzoate, but only respond to the highest dose o f sCCK-8 administered after the higher dose of estradiol benzoate ( fig.…”

Section: Effects O F Neonatal Castration or Testosterone Treatmentmentioning

confidence: 99%

Development of the Limbic-Hypothalamic Cholecystokinin Circuit: A Model of Sexual Differentiation pp. 23–34

Micevych¹,

Ulibarri²

1992

Dev Neurosci

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Reproductive behavior is the final outcome of the integration of appropriate gonadal hormonal stimulation with olfactory and somatic cues by the steroid-sensitive limbic-hypothalamic neural circuit. Gonadal hormones sexually differentiate the structure and neurochemistry of this circuit during development. In adulthood, gonadal steroids continue to regulate the behavioral response of the animal through their effects on intercellular signalling in this limbic-hypothalamic circuit. Recently, the neuropeptide cholecystokinin has been demonstrated to be an important intercellular messenger, expression, distribution, levels, and receptors of which are regulated both during development and adulthood by the gonadal steroid environment. Studies on the development of sex differences using the cholecystokinin component of this circuit as a model have yielded insight into how gonadal steroids modulate the neurochemistry of the reproductively relevant limbic-hypothalamic circuit. Concentrating on this circuit and its role in reproduction, we will review the data about gonadal steroid effects on the distribution, expression, development, and physiology of cholecystokinin and its receptors.

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Female sexual behavior in male rats: Effect of hour of castration at birth

Cited by 57 publications

References 15 publications

Living or dying in three quarter time: Neonatal orchestration of hippocampal cell death pathways by androgens and excitatory GABA

Living or dying in three quarter time: Neonatal orchestration of hippocampal cell death pathways by androgens and excitatory GABA

Effect of Progesterone on the Testosterone and Estradiol Levels in the Hypothalamus of Neonatal Rats

Development of the Limbic-Hypothalamic Cholecystokinin Circuit: A Model of Sexual Differentiation pp. 23–34

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