Paucity of c-fos expression in the medial preoptic area of prenatally stressed male rats following exposure to sexually receptive females

Humm, J.; Lambert, Kelly G.; Kinsley, Craig Howard

doi:10.1016/0361-9230(95)00011-9

Cited by 14 publications

(11 citation statements)

References 31 publications

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“…Additionally, the absence of testosterone or its metabolites feminized sexually dimorphic structures [272]. In fact, PS has been found to alter the sexual dimorphism of brain structures in male rats; these animals exhibit a diminished number of neurons in the spinal nucleus bulbocavernosus [123] and a decrease in c-fos activity within the medial preoptic area [146]. However, these PS-induced effects on neural differentiation are specific since several structures like the medial amygdala are not affected by PS-evoked alterations of the prenatal testosterone peak [157].…”

Section: Sexual Brain Differentiationmentioning

confidence: 99%

Impact of Prenatal Stress on Neuroendocrine Programming

Viltart

Vanbesien-Mailliot

2007

The Scientific World JOURNAL

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Since life emerged on the Earth, the development of efficient strategies to cope with sudden and/or permanent changes of the environment has been virtually the unique goal pursued by every organism in order to ensure its survival and thus perpetuate the species. In this view, evolution has selected tightly regulated processes aimed at maintaining stability among internal parameters despite external changes, a process termed homeostasis. Such an internal equilibrium relies quite heavily on three interrelated physiological systems: the nervous, immune, and endocrine systems, which function as a permanently activated watching network, communicating by the mean of specialized molecules: neurotransmitters, cytokines, and hormones or neurohormones. Potential threats to homeostasis might occur as early as during in utero life, potentially leaving a lasting mark on the developing organism. Indeed, environmental factors exert early-life influences on the structural and functional development of individuals, giving rise to changes that can persist throughout life. This organizational phenomenon, encompassing prenatal environmental events, altered fetal growth, and development of long-term pathophysiology, has been named early-life programming. Over the past decade, increased scientific activities have been devoted to deciphering the obvious link between states of maternal stress and the behavioral, cognitive, emotional, and physiological reactivity of the progeny. This growing interest has been driven by the discovery of a tight relationship between prenatal stress and development of short- and long-term health disorders. Among factors susceptible of contributing to such a deleterious programming, nutrients and hormones, especially steroid hormones, are considered as powerful mediators of the fetal organization since they readily cross the placental barrier. In particular, variations in circulating maternal glucocorticoids are known to impact this programming strongly, notably when hormonal surges occur during sensitive periods of development, so-called developmental windows of vulnerability. Stressful events occurring during the perinatal period may impinge on various aspects of the neuroendocrine programming, subsequently amending the offspring's growth, metabolism, sexual maturation, stress responses, and immune system. Such prenatal stress-induced modifications of the phenotypic plasticity of the progeny might ultimately result in the development of long-term diseases, from metabolic syndromes to psychiatric disorders. Yet, we would like to consider the outcome of this neuroendocrine programming from an evolutionary perspective. Early stressful events during gestation might indeed shape internal parameters of the developing organisms in order to adapt the progeny to its everyday environment and thus contribute to an increased reproductive success, or fitness, of the species. Moreover, parental care, adoption, or enriched environments after birth have been shown to reverse negative long-term consequences of a disturbed ...

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Section: Sexual Brain Differentiationmentioning

confidence: 99%

Impact of Prenatal Stress on Neuroendocrine Programming

Viltart

Vanbesien-Mailliot

2007

The Scientific World JOURNAL

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“…PS, which demasculinizes male rats, 3,4,6 appears to alter nNOS in adult male rats in both mPOA and bAM. The number of neurons, as defined primarily by perikarya, expressing nNOS-IR is lower in PS animals in both mPOA and bAM.…”

Section: Discussionmentioning

confidence: 91%

“…1,2,8 The medial preoptic area (mPOA) and basolateral amygdala (bAM) regulate, respectively, sexual and aggressive behavior. 4,5,7,9,10 Given that PS affects both aggression and sexual behavior, the current work examines NO (through its rate-limiting enzyme neuronal NO synthase [nNOS]) in the mPOA and bAM of PS male rats.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Stress‐induced Modifications of Neuronal Nitric Oxide Synthase in Amygdala and Medial Preoptic Area

Miller

Mueller

Gifford

et al. 1999

Annals of the New York Academy of Sciences

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“…One possibility is that the threshold changes involve a diminished concentration of neural androgen receptors, particularly within the medial preoptic area (MPOA). The MPOA has been identified as a pivotal site within the brain circuitry controlling male copulatory patterns (see review by Meisel and Sachs, 1994) and c-fos expression in this site is diminished in prenatally stressed males exposed to estrous females in adulthood (Humm, Lambert, and Kinsley, 1995). The display of male sexual behaviors in the rat requires activation of neural androgen receptors (Vagell and McGinnis, 1998).…”

Section: Possible Involvement Of the Medial Preopticmentioning

confidence: 99%