Changes in Testicular Weight and Serum Gonadotropin and Testosterone Levels before, during, and after Birth in the Perinatal Rat*

Corbier, P.; Kerdelhué, B.; Picon, R.; Roffi, J

doi:10.1210/endo-103-6-1985

Cited by 179 publications

(61 citation statements)

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“…Hormone measurements were made in whole body homogenates of individual foetuses in the interest of economy instead of in pooled plasma from numerous males or females killed at each embryonic age. Studies using rats (16)(17)(18); MJ Baum, P Woutersen and AK Slob, unpublished results) have shown that the profile of sex differences in whole body androgen content parallels closely that measured in pools of plasma taken over the last week of gestation as well as over the first 24 h after birth. Using both methods male rats had significantly higher levels of androgen than females only on gestational Days El8 and El9 as well as 1 to 3 h after birth.…”

Section: Perinatal Profile Of Androgen Secretion In Ferretsmentioning

confidence: 74%

Steroidal Control of Behavioural, Neuroendocrine and Brain Sexual Differentiation: Studies in a Carnivore, the Ferret

Baum

Carroll

Cherrv

et al. 1990

J Neuroendocrinology

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More than 30 years have passed since the publication ( I ) showing that transplacental administration of testosterone to female guinea-pigs caused permanent changes in their ability to exhibit reproductive behaviours in response to ovarian steroids in adulthood. Over the intervening years articles have appeared which have extended this type of observation to numerous other mammalian species, including rat, hamster, gerbil, mouse, dog, ferret, pig, sheep, rhesus monkey, and marmoset (2, 3). In many instances inferences have been made about the probable existence of steroid-induced changes in the structure and function of the nervous system which underlie these changes in behaviour. These so-called 'organizational' effects of perinatal steroid exposure on the developing nervous system are often distinguished from the later 'activational' effects of these same steroids on the expression of sociosexual behaviours in adulthood. The number of different mammalian species used for mechanistic studies on the organizational effects of steroids, such as determining the precise perinatal timing of hormone action, the identity of the steroid(s) responsible for behavioural sexual differentiation, and the neural sites of steroid action, has been relatively small, and generally restricted to rodents. In the late 1970's sex steroids acting during development were first implicated in the differentiation of sexually dimorphic telencephalic structures in passerine song birds which control singing associated with courtship (4, 5). Since this early work, numerous studies have exploited the canary and zebra finch to explore mechanisms of steroid action in controlling the ontogeny of song in the male and the underlying changes in the nervous system. Other studies using the rat have explored in detail the role of androgen and oestrogen in controlling the differentiation in males of patterns of reproductive behaviour (2) as well as aspects of neural sex dimorphisms in the preoptic area/anterior hypothalamus (POA/AH) (6) and in the lumbar spinal cord (7). The concentration of mechanistic (behavioural, biochemical, neuroanatomical) studies of steroidal effects on sexually dimorphic behavioural potential in a few avian and rodent species is understandable, in light of their relative availability, low expense, and rapid time-course of neural development.Despite the substantial progress already made using these lower vertebrate models in promoting our understanding of how sex steroids influence neural and behavioural development, extrapolation of the results obtained in these studies to higher mammals including man cannot occur in the absence of some degree of empirical verification. Obviously, experimental manipulations of steroidal exposure during the development of human subjects would be unethical, thus we are left with experiments of nature (e.g. congenital adreno-genital syndrome,androgen insensitivity syndrome, and Sa-reductase deficient pseudohermaphroditism; details in later sections) with which to ask questions about the role of sex...

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Section: Perinatal Profile Of Androgen Secretion In Ferretsmentioning

confidence: 74%

Steroidal Control of Behavioural, Neuroendocrine and Brain Sexual Differentiation: Studies in a Carnivore, the Ferret

Baum

Carroll

Cherrv

et al. 1990

J Neuroendocrinology

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“…Of six litters used for this treatment group, four were bom between 10.00 and 14.00 h and were cas trated immediately after parturition, within 1-2 h of the birth of the first pup. Thus, they were castrated before the peak of the 'birth surge' of T which occurs 2 h after partu rition [32], The AVPv volumes of all of these animals (18 of the 24 castrates) were well within the range of 1 SD of the mean for the entire group of neonatally castrated males.…”

Section: Discussionmentioning

confidence: 96%

Structural Sexual Dimorphisms in the Anteroventral Periventricular Nucleus of the Rat Hypothalamus Are Sensitive to Gonadal Steroids Perinatally, but Develop Peripubertally

Davis¹,

Shryne²,

Gorski³

1996

Neuroendocrinology

121

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The volume of the anteroventral periventricular nucleus (AVPv) of the rat hypothalamus is larger in females than in males. A preliminary study from this laboratory found that this sexual dimorphism develops between days 30 and 91. The present study was designed to confirm and extend these findings and to determine the role of endogenous gonadal steroids in the development of the AVPv postnatally. The results indicate that the sexual dimorphism in AVPv volume arises between days 30 and 40 and that the length of the nucleus becomes sexually dimorphic between days 60 and 80. Additionally, both AVPv volume and length increased between days 30 and 80 in females. Castration of male rats on the day of birth sex-reversed AVPv volume in adulthood and AVPv length was sex-reversed by castration of males 5 days after birth; ovariectomy of females at these ages had no effect on either parameter. Moreover, in both males and females, AVPv volume and length were unaffected by gonadectomy at later ages. That the AVPv appears to be influenced by testicular hormones neonatally, but changes structurally around the time of puberty in females, clearly challenges current concepts of sexual differentiation that limit the process to the early postnatal period.

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“…A neonatal surge in plasma testosterone shortly after birth has been well documented to occur in both male rats and humans [1, 2]. This increase in testosterone at a critical period of development has been implicated in the long-term modulation of a number of central nervous system (CNS) functions including play and sexual behavior, dopaminergic neurotransmission and responses to early CNS lesions [3,4,5,6,7,8].…”

Section: Introductionmentioning

confidence: 99%

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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Background/Aims: Global birth hypoxia in rats has been shown to produce long-term changes in central nervous system functions, known to be influenced by neonatal testosterone secretion. Birth hypoxia alters levels of several circulating hormones, but it is unknown if it affects neonatal testosterone. Methods: Using a rat model of acute global hypoxia during cesarean section (C-section) birth, this study tested whether birth hypoxia affects neonatal testosterone. We then evaluated whether the observed hypoxia-induced changes in neonatal testosterone may be mediated via N-methyl-D-aspartate (NMDA) receptor activation and/or altered luteinizing hormone (LH), adrenocorticotropic hormone (ACTH) or corticosterone levels. Longer-term effects of birth hypoxia on testosterone-related function were also assessed. Results: Rats born by C-section + 15 min of anoxia had significantly higher plasma testosterone at 2 and 3 h after birth compared to controls born either vaginally or by C-section. Administration of an NMDA receptor antagonist at birth increased neonatal testosterone in both anoxic pups and controls. Pups exposed to birth anoxia under hypothermic conditions also showed increased neonatal testosterone. Circulating LH, follicle-stimulating hormone and corticosterone in neonates, and testosterone at adulthood were unaffected by birth hypoxia. However, plasma ACTH was significantly increased in anoxic neonates at 2 h after birth. Birth condition had no effect on anogenital distance or juvenile play behavior. Conclusion: It is concluded that birth hypoxia augments plasma testosterone during the critical period of the neonatal testosterone surge, by a mechanism that is independent of NMDA-mediated LH secretion, but may involve increased circulating ACTH.

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Changes in Testicular Weight and Serum Gonadotropin and Testosterone Levels before, during, and after Birth in the Perinatal Rat*

Cited by 179 publications

References 0 publications

Steroidal Control of Behavioural, Neuroendocrine and Brain Sexual Differentiation: Studies in a Carnivore, the Ferret

Steroidal Control of Behavioural, Neuroendocrine and Brain Sexual Differentiation: Studies in a Carnivore, the Ferret

Structural Sexual Dimorphisms in the Anteroventral Periventricular Nucleus of the Rat Hypothalamus Are Sensitive to Gonadal Steroids Perinatally, but Develop Peripubertally

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

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