Year: 2010
Type: dissertation
Abstract: Adverse experiences during early life causes alterations in the development of the central nervous system structures that may result in abnormal functioning of the brain.It is well known that, in humans, adverse early-life experiences such as social separation, deprivation, maternal neglect and abuse increase the risk of developing psychiatric disorders, such as depression, later in life.We used maternal separation in the rat as a model for early life stress to firstly determine how different brain systems are dysregulated by this stressful experience and additional chronic or acute stress during adulthood.Rat pups were separated from their mothers on postnatal day 2-14 for 3 hours per day while control rats were normally reared.The behavior, stress response, neurotrophin, apoptotic marker and serotonin levels in the ventral hippocampus, striatum and frontal cortex were measured during adulthood.A different group of maternally separated rats were allowed chronic voluntary exercise and similar measurements were done to determine whether exercise was able to normalize the deficits caused by early life stress.Differentially expressed cytosolic proteins of the ventral hippocampus of maternally separated rats versus normally reared rats were also identified.Protein expression levels of maternally separated rats that received chronic voluntary exercise or escitalopram treatment were subsequently determined to unravel the mechanism of therapeutic action for these two interventions.We found that maternal separation increased the baseline corticosterone response of rats and induced a blunted adrenocorticotropin hormone after acute restraint stress.Baseline neurotrophin levels were significantly decreased in the ventral hippocampus.Maternal separation followed by chronic restraint stress during adulthood resulted in increased depressive-like behavior compared to control rats.Maternal separation alone or followed by acute restraint Table of contents
Author: Lelanie Marais
Language: English
Subfield: Behavioral Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2113715613