Morphological Responses of Excitatory Prelimbic and Orbitofrontal Cortical Neurons to Excess Corticosterone in Adolescence and Acute Stress in Adulthood.

Considerable evidence indicates that chronic stress and excess glucocorticoids induce neuronal remodeling in prefrontal cortical (PFC) regions. Adolescence is also characterized by a structural reorganization of PFC neurons, yet interactions between stress- and age-related structural plasticity are still being determined. We quantified dendritic spine densities on apical dendrites of excitatory neurons in the medial prefrontal cortex, prelimbic subregion (PL).

Glucocorticoid-sensitive ventral hippocampal-orbitofrontal cortical connections support goal-directed action - Curt Richter Award Paper 2019.

In an ever-changing and often ambiguous environment, organisms must use previously learned associations between antecedents and outcomes to predict future associations and make optimal choices. Chronic stress can impair one's ability to flexibly adjust behaviors when environmental contingencies change, particularly in cases of early-life stress. In mice, exposure to elevated levels of the primary stress hormone, corticosterone (CORT), during early adolescence is sufficient to impair response-outcome decision making later in life, biasing response strategies towards inflexible habits.

Action-Outcome Expectancies Require Orbitofrontal Neurotrophin Systems in Naïve and Cocaine-Exposed Mice.

Cocaine use during adolescence decreases the likelihood that individuals will seek treatment for recurrent drug use. In rodents, developmental cocaine exposure weakens action-consequence decision-making, causing a deferral to familiar, habit-like behavioral response strategies. Here, we aimed to improve action-outcome decision-making.

Prefrontal cortical trkB, glucocorticoids, and their interactions in stress and developmental contexts.

The tropomyosin/tyrosine receptor kinase B (trkB) and glucocorticoid receptor (GR) regulate neuron structure and function and the hormonal stress response. Meanwhile, disruption of trkB and GR activity (e.g.

Adolescent Corticosterone and TrkB Pharmaco-Manipulations Sex-Dependently Impact Instrumental Reversal Learning Later in Life.

Early-life trauma can increase the risk for, and severity of, several psychiatric illnesses. These include drug use disorders, and some correlations appear to be stronger in women. Understanding the long-term consequences of developmental stressor or stress hormone exposure and possible sex differences is critically important.

Regulation of actions and habits by ventral hippocampal trkB and adolescent corticosteroid exposure.

In humans and rodents, stress promotes habit-based behaviors that can interfere with action-outcome decision-making. Further, developmental stressor exposure confers long-term habit biases across rodent-primate species. Despite these homologies, mechanisms remain unclear.

Oral self-administration of EtOH: sex-dependent modulation by running wheel access in C57BL/6J mice.

Background: The effects of stress, including neuroendocrine and behavioral sequelae aimed at maintaining homeostasis, are associated with increased alcohol consumption. Because both stress and drinking are multifactorial, the mechanisms underlying the relationship are difficult to elucidate. We therefore employed an animal model investigating the influence of blocked access to a running wheel on drinking in C57BL/6J (B6) mice.

β-endorphin modulates the effect of stress on novelty-suppressed feeding.

Although stress is implicated in the pathophysiology of mood and anxiety disorders, not all individuals who suffer stressful life events develop psychopathology. Differential susceptibility to stress may be influenced by genetically mediated differences in hypothalamic-pituitary-adrenal (HPA) axis activity and moderation of the stress response by the opioid peptide β-endorphin (β-E). The present study investigated genetic contributions to coping behavior by examining anxious behavior of transgenic mice with varying capacities to synthesize β-E [B6.

Beta-endorphin mediates behavioral despair and the effect of ethanol on the tail suspension test in mice.

Background: The opioid peptide beta-endorphin (beta-E) is synthesized and released in response to stressful stimuli as well as acute alcohol administration. The release of beta-E following exposure to an inescapable aversive situation may mediate behaviors that contribute to allostasis of the stress response. The present study examines the effects of beta-E on immobility in assays involving inescapable stress, both under basal conditions and after acute administration of EtOH.