Sleep and Behavior in Cross-Fostering Rats: Developmental and Sex Aspects

Abstract

Study Objective: Adverse early-life events induce behavioral psychopathologies and sleep changes in adulthood. In order to understand the molecular level mechanisms by which the maltreatment modifies sleep, valid animal models are needed. Changing pups between mothers at early age (cross-fostering) may satisfyingly model adverse events in human childhood. Methods: Cross-fostering (CF) was used to model mild early-life stress in male and female Wistar rats. Behavior and BDNF gene expression in the basal forebrain (BF), cortex, and hypothalamus were assessed during adolescence and adulthood. Spontaneous sleep, sleep homeostasis, and BF extracellular adenosine levels were assessed in adulthood. Results: CF rats demonstrated increased number of REM sleep onsets in light and dark periods of the day. Total REM and NREM sleep duration was also increased during the light period. While sleep homeostasis was not severely affected, basal level of adenosine in the BF of both male and female CF rats was lower than in controls. CF did not lead to considerable changes in behavior. Conclusions: Even when the consequences of adverse early-life events are not observed in tests for anxiety and depression, they leave a molecular mark in the brain, which can act as a vulnerability factor for psychopathologies in later life. Sleep is a sensitive indicator for even mild early-life stress.

The effects of maternal risk factors during pregnancy on the onset of sleep difficulties in infants at 3 months old

“…In fact, both animal and human studies have found prenatal maternal anxiety and depression to be associated with sleep difficulties at early ages. For instance, experimental animal research shows that prenatal and early postnatal stress are associated with long‐lasting structural sleep changes in the offspring mimicking those reported in depression (Santangeli et al., ). The underlying mechanism of such long‐term effects of prenatal conditions is believed to be the inhibition of the 11ß‐hydroxysteroid dehydrogenase type 2 (HSD2) placental enzyme, which is responsible for inactivation of excessive maternal glucocorticoids (Harris & Seckl, ).…”

Environmental Enrichment During Adolescence Mitigates Cognitive Deficits and Alcohol Vulnerability due to Continuous and Intermittent Perinatal Alcohol Exposure in Adult Rats

“…The day when pregnancy was confirmed by vaginal smear (Cannizzaro et al, 2008 ; Plescia et al, 2014b ), designed as gestational day 1 (GD1), eight female rats were randomly selected from each experimental group ( n = 12), housed in standard maternity cages, filled with wood shavings. Dams were inspected twice daily for delivery until the day of parturition, considered as postnatal day 0 (PND 0); dams and litters were kept in a nursery (24 ± 2°C) and not separated until weaning, in order to model the human condition and avoid confounding factors (Subramanian, 1992 ; Wilson et al, 1996 ; Santangeli et al, 2016 ). Mean alcohol consumption at 1 h and 24 h by CAD and IAD rat dams during pre-conception period, gestation, and lactation was recorded and reported as g/kg ± SEM.…”

Pre-conceptional and Peri-Gestational Maternal Binge Alcohol Drinking Produces Inheritance of Mood Disturbances and Alcohol Vulnerability in the Adolescent Offspring

“…Female rats underwent the self-administration procedure throughout pregnancy, accordingly to the respective two-bottle choice paradigm. Dams were inspected twice daily for delivery until the day of parturition, considered as postnatal day 0 (PND 0); dams and litters were kept in a nursery (24 ± 2°C) and not separated until weaning, in order to avoid confounding effects due to cross-fostering procedure [ 43 – 45 ] and model the human condition.…”