Maternal Exposure to Low Levels of Corticosterone during Lactation Protects the Adult Offspring against Ischemic Brain Damage

Abstract

A growing body of evidence underscores the importance of early life events as predictors of health in adulthood. Abnormalities in maternal care or other forms of early postnatal stress induce long-term changes in behavior and influence the vulnerability to illnesses throughout life. Some of these changes may be produced by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, which is invariably associated with stress. We used a model in which neonate rats are fed by mothers drinking water supplemented with 0.2 mg/ml corticosterone, the main glucocorticoid hormone in rodents. Plasma corticosterone levels increased in the dams to an extent similar to that induced by a mild stress. Corticosterone-treated dams also showed an increase in maternal care. Remarkably, adult rats that had been nursed by corticosterone-treated mothers were protected against neuronal damage and cognitive impairment produced by transient global brain ischemia. Neuroprotection was associated with a reduced HPA response to ischemia and was primarily decreased when corticosterone was injected at a dose that eliminated any difference in endogenous corticosterone levels between rats raised by mothers supplemented with corticosterone and their matched controls. These data suggest that an increased maternal care protects the offspring against ischemic neuronal damage and that at least a component of neuroprotection is mediated by a reduced response of the HPA axis to ischemia.

Microglial VEGF Receptor Response Is an Integral Chemotactic Component in Alzheimer's Disease Pathology

“…The number of Iba-1 or NeuN(ϩ) cells in the CA1 region was quantified at three hippocampal sections. To keep the consistency between the selected sections, a rectangular box (0.4 ϫ 0.3 mm) was centered over the CA1 cell layer beginning 1.6 mm lateral to the midline in each image as previously described (Casolini et al, 2007). For quantification of migrating enhanced green fluorescent protein (EGFP)-expressing microglia after transplantation, the number of EGFP(ϩ) microglia were counted within rectangular areas (0.3 ϫ 0.2 mm) for three different regions (centered 600, 1200, and 1800 m away from the transplantation site).…”

Food restriction enhances visual cortex plasticity in adulthood

“…We addressed this issue pharmacologically mimicking the every other day elevation of blood corticosterone caused by our protocol of FR. We treated a group of rats with a low dose of corticosterone in drinking water on alternate days for 4 weeks, as previously reported in rodents [26][27][28] , and we tested visual cortex plasticity evaluating the effects of 1 week of MD on OD distribution of cortical neurons. We found a significant shift of C/I VEP ratio in favour of the open eye in the visual cortex of MD rats treated with corticosterone (C/I VEP ratio = 1.22 ± 0.07; n = 5; one-way ANOVA P < 0.001; post hoc HolmSidak test CTL versus FR P < 0.001; CTL versus Cort P < 0.001; Cort versus FR P = 0.826; Fig.…”

Changes in anxiety and cognition due to reproductive experience: A review of data from rodent and human mothers

“…Proper maternal behavior is critical for offspring, as pups of mothers who spend less time with their pups have abnormal social behavior, higher anxiety-like behavior on the elevated zero maze, and higher corticosterone levels as adults (Coutellier et al, 2008). Similarly, the adult offspring of corticosterone-treated mothers (15 mg/rat) are protected against the neuronal damage and cognitive impairment normally produced with transient global ischemia (Casolini et al, 2007). However, treatment with high levels of corticosterone (40 mg/kg) can increase time off the nest and decrease nursing (Brummelte et al, 2006), indicating an inverted U-curve facilitatory effect of corticosterone on maternal behavior.…”