Parental enriched environment: A look through key temporary windows.

Environmental enrichment is a widely used experimental manipulation that physically, cognitively and socially stimulates individuals. It has a great variety of long-term effects at neuroanatomical, neurochemical, and behavioral level; however, the influence of parental environmental enrichment during gestation and pregestation on the development of the offspring and on the mother's behavior has been poorly explored. This article presents a review of the literature from the year 2000 about the effects of maternal and paternal environmental enrichment on the behavioral, endocrine, and neural systems of offspring and parents.

Animal models of postpartum depression revisited.

Postpartum depression (PPD) is a heterogeneous mood disorder and the most frequent psychiatric complication of the postnatal period. Given its potential long-lasting repercussions on the well-being of the mother and the infants, it should be a priority in public health. In spite of efforts devoted to clinical investigation and preclinical studies, the underlying neurobiological mechanisms of this disorder remain unknown in detail.

Postweaning Enriched Environment Enhances Cognitive Function and Brain-Derived Neurotrophic Factor Signaling in the Hippocampus in Maternally Separated Rats.

Adverse environments during early life may lead to different neurophysiological and behavioral consequences, including depression and learning and memory deficits that persist into adulthood. Previously, we demonstrated that exposure to an enriched environment during adolescence mitigates the cognitive impairment observed after maternal separation in a task-specific manner. However, underlying neural mechanisms are still not fully understood.

Estradiol-dependent axogenesis and Ngn3 expression are determined by XY sex chromosome complement in hypothalamic neurons.

Hypothalamic neurons show sex differences in neuritogenesis, female neurons have longer axons and higher levels of the neuritogenic factor neurogenin 3 (Ngn3) than male neurons in vitro. Moreover, the effect of 17-β-estradiol (E2) on axonal growth and Ngn3 expression is only found in male-derived neurons. To investigate whether sex chromosomes regulate these early sex differences in neuritogenesis by regulating the E2 effect on Ngn3, we evaluated the growth and differentiation of hypothalamic neurons derived from the "four core genotypes" mouse model, in which the factors of "gonadal sex" and "sex chromosome complement" are dissociated.

Gonadal hormone-independent sex differences in GABA receptor activation in rat embryonic hypothalamic neurons.

Background And Purpose: GABA receptor functions are dependent on subunit composition, and, through their activation, GABA can exert trophic actions in immature neurons. Although several sex differences in GABA-mediated responses are known to be dependent on gonadal hormones, few studies have dealt with sex differences detected before the critical period of brain masculinisation. In this study, we assessed GABA receptor functionality in sexually segregated neurons before brain hormonal masculinisation.

Sex differences in depolarizing actions of GABA receptor activation in rat embryonic hypothalamic neurons.

GABA receptor activation exerts trophic actions in immature neurons through depolarization of resting membrane potential. The switch to its classical hyperpolarizing role is developmentally regulated. Previous results suggest that a hormonally biased sex difference exists at the onset of the switch in hypothalamic neurons.

Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability.

Amyotrophic lateral sclerosis (ALS) is a devastating paralytic disorder caused by dysfunction and degeneration of motoneurons starting in adulthood. Recent studies using cell or animal models document that astrocytes expressing disease-causing mutations of human superoxide dismutase 1 (hSOD1) contribute to the pathogenesis of ALS by releasing a neurotoxic factor(s). Neither the mechanism by which this neurotoxic factor induces motoneuron death nor its cellular site of action has been elucidated.

Sex chromosome complement contributes to sex differences in bradycardic baroreflex response.

To investigate whether sex chromosome complement modulates bradycardic baroreflex response and contributes to the angiotensin II-bradycardic baroreflex sex differences, we used the four core genotype mouse model in which the effect of gonadal sex and sex chromosome complement is dissociated, allowing comparisons of sexually dimorphic traits among XX and XY females, as well as in XX and XY males. In conscious gonadectomized (GDX) MF1 transgenic mice we evaluated baroreflex regulation of heart rate in response to changes in blood pressure evoked by phenylephrine (1 mg/mL), angiotensin II (100 μg/mL), and sodium nitroprusside (1 mg/mL). The administration of phenylephrine in GDX-XY females resulted in a significantly lower baroreflex response when compared with the other genotypes (in beats · min(-1) · mm Hg(-1) [slopes of regression lines for GDX-XY females -3.