Impaired Energy Metabolism and Disturbed Dopamine and Glutamate Signalling in the Striatum and Prefrontal Cortex of the Spontaneously Hypertensive Rat Model of Attention-Deficit Hyperactivity Disorder.

Attention deficit hyperactivity disorder (ADHD) is a heterogeneous behavioural disorder that affects 3-15 % of children worldwide. Spontaneously hypertensive rats (SHR) display the major symptoms of ADHD (hyperactivity, impulsivity and poor performance in tasks that require sustained attention) and are widely used to model the disorder. The present study aimed to test the hypothesis that SHR have a diminished capacity to generate ATP required for rapid synchronized neuronal firing, failure of which might lead to disturbances in neurotransmission that could contribute to their ADHD-like behaviour.

Exercise normalizes altered expression of proteins in the ventral hippocampus of rats subjected to maternal separation.

Many studies have reported on the detrimental effects of early life adversity and the beneficial effects of exercise on brain function. However, the molecular mechanisms that underpin these various effects remain poorly understood. The advent of advanced proteomic analysis techniques has enabled simultaneous measurement of protein expression in a wide range of biological systems.

Exercise increases BDNF levels in the striatum and decreases depressive-like behavior in chronically stressed rats.

Early life stress in humans can affect the development of neurons and neurotransmitter systems and predispose an individual to the subsequent development of depression. Similarly, in rats, maternal separation causes anxiety and depressive-like behavior and decreased corticosterone levels. Patients receiving pharmacological treatment for depression often experience negative side-effects or do not respond optimally and therefore the use of exercise as alternative antidepressant treatment is investigated.

A proteomic analysis of the ventral hippocampus of rats subjected to maternal separation and escitalopram treatment.

Early life stress is known to predispose humans to the development of depression. Developmental stress has been shown to cause various changes in neurotransmitter systems, neurotrophin expression and the hypothalamic pituitary adrenal-axis in the rat brain. The aim of this study was to identify which cytosolic proteins are altered by maternal separation, as a model for depression, as well as by chronic antidepressant treatment.

Maternal separation of rat pups increases the risk of developing depressive-like behavior after subsequent chronic stress by altering corticosterone and neurotrophin levels in the hippocampus.

Children that are abused have an increased risk for developing psychiatric disorders later in life, because of the negative effects of stress on the developing brain. We used a maternal separation model in rats to see how neurotrophins, stress hormones, behavior and the anti-oxidant potential of serum are affected. Rat pups were separated from their mothers for 3h/day on days 2-14.

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

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).

Developmental trauma is associated with behavioral hyperarousal, altered HPA axis activity, and decreased hippocampal neurotrophin expression in the adult rat.

Effects of early-life trauma on adult behavioral responses, corticosterone (CORT) concentration, and levels of nerve growth factor (NGF), brain-derived neutrophic factor (BDNF), and neurotrophin-3 (NT-3) in hippocampus and frontal cortex were investigated. Traumatized animals showed an increase in rearing in both the elevated plus maze and open field after adult restress, higher basal levels of CORT, lower levels of BDNF in dorsal hippocampus, and lower levels of NT-3 in dorsal and ventral hippocampus. Trauma-related behavioral hyperarousal and altered hypothalamic-pituitary-adrenal (HPA) axis activity may be mediated by decreases in hippocampal neurotrophin expression.

Psychopharmacology of maternal separation anxiety in vervet monkeys.

Maternal separation in non-human primates has been proposed as a model of early adversity. The symptoms of separation anxiety were studied in vervet monkeys, during the weaning period, when psychotropic medications were administered. The control group received a normal diet and treatment groups received citalopram, reboxetine or lamotrigine in their food daily.

Early maternal separation followed by later stressors leads to dysregulation of the HPA-axis and increases in hippocampal NGF and NT-3 levels in a rat model.

Early adverse life events, followed by subsequent stressors, appear to increase susceptibility for subsequent onset of psychiatric disorders in humans. The molecular mechanisms that underlie this phenomenon remain unclear, but dysregulation of the HPA axis and alterations in neurotrophic factors have been implicated. The present study investigated the effects in rodents of early maternal separation, followed by stress in adolescence and adulthood on later HPA-axis activity and hippocampal neurotrophin levels (brain-derived neurotrophic factor, nerve growth factor, and neurotrophin-3).