Early maternal separation alters the response to traumatization: Resulting in increased levels of hippocampal neurotrophic factors

Date
2007
Authors
Faure J.
Uys J.D.K.
Marais L.
Stein D.J.
Daniels W.M.U.
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Volume Title
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Abstract
Early life adversity predisposes individuals to the development of psychopathology in later life, especially depression and anxiety disorders. Prior history of stressors may also be a vulnerability factor for developing posttraumatic stress disorder (PTSD) in response to trauma. We examined the mechanisms underlying this phenomenon by employing two animal stress models, early maternal separation followed by later time-dependent sensitization (TDS). In animals exposed to adult TDS, those with prior early adversity did not differ from controls on tests of anxiety (elevated plus maze, open field), or HPA function (ACTH and corticosterone levels). However, those with prior early adversity had increased levels of neurotrophic factors (BDNF, NGF and NT-3) in both the dorsal and ventral hippocampus. Although early adversity is known to be associated with negative effects on neuronal function, it may also be associated with an increased ability to respond to subsequent stressors with compensatory mechanisms such as increased neurotrophic factor release. © 2007 Springer Science+Business Media, LLC.
Description
Keywords
brain derived neurotrophic factor, corticosterone, corticotropin, nerve growth factor, neurotrophic factor, neurotrophin 3, animal experiment, anxiety, article, behavior, controlled study, hippocampus, hypothalamus hypophysis adrenal system, injury, life stress, male, maternal deprivation, maze test, nerve function, nonhuman, open field test, rat, sensitization, Adrenocorticotropic Hormone, Animals, Brain-Derived Neurotrophic Factor, Corticosterone, Hippocampus, Hypothalamo-Hypophyseal System, Male, Maternal Deprivation, Maze Learning, Nerve Growth Factor, Nerve Growth Factors, Neurotrophin 3, Pituitary-Adrenal System, Rats, Rats, Sprague-Dawley, Stress, Psychological, Animalia
Citation
Metabolic Brain Disease
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2