The resilience of adolescent male rats to acute stress-induced delayed anxiety is age-related and glucocorticoid release-dependent.

Studies investigated how stressful experiences modulate physiological and behavioral responses and the consequences of stress-induced corticosterone release in anxiety-like behavior. Adolescence is crucial to brain maturation, and several neurobiological changes in this period lead individuals to increased susceptibility or resilience to aversive situations. Despite the effects of stress in adults, information about adolescents' responses to acute stress is lacking.

Imbalance in the ratio between mineralocorticoid and glucocorticoid receptors and neurodegeneration in the dentate gyrus of aged dogs.

Background And Aim: Cortisol binds to mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) found in the hippocampus. The balanced expression of these receptors is essential to neuronal survival as MR and GR activations have antiapoptotic and proapoptotic effects, respectively. Given the aging changes in dogs' dentate gyrus (DG) and the possible involvement of cortisol receptors in this process, this study aimed to evaluate the expression of MR and GR and neuronal degeneration in this hippocampal region of aged dogs.

Exploring the light/dark box test: Protocols and implications for neuroscience research.

Background: Knowledge on the neurobiological systems underlying psychiatric disorders has considerably evolved due to findings on basic research using animal models. Anxiety-like behaviors in rodents are widely explored in neuroethological apparatuses, such as the light-dark box (LDB) test through different protocols, which have been shown to influence the behavioral outcomes and probably the activation of the hypothalamic-pituitary-adrenal (HPA) axis.

New Method: Adult male Wistar rats were submitted to LDB in different room illumination conditions (25/0, 65/0 and/or 330/0 lux), initial positioning in the LDB compartments and previous stressful experience in the Elevated Plus Maze (EPM) or restraint stress (RS).

Predator fear memory depends on glucocorticoid receptors and protein synthesis in the basolateral amygdala and ventral hippocampus.

Previous studies have suggested that the basolateral amygdala (BLA) and the ventral hippocampus (VH) are critical sites for predator-related fear memory. Predator exposure is an intense emotional experience and should increase plasmatic corticosterone likely to modulate the emotion-related memories. However, it is unclear whether the BLA and VH harbor plastic events underlying predator-related fear memory storage and how molecular and endocrine mechanisms interact to modulate memory to the predatory threat.

Exposure to Running Wheels Prevents Ethanol Rewarding Effects: The Role of CREB and Deacetylases SIRT-1 and SIRT-2 in the Nucleus Accumbens and Prefrontal Cortex.

Alcohol use disorder is one of the most prevalent addictions, strongly influenced by environmental factors. Voluntary physical activity (VPA) has proven to be intrinsically reinforcing and we hypothesized that, as a non-drug reinforcer, VPA could mitigate ethanol-induced rewarding effects. The transcriptional factor cAMP response element binding protein (CREB), and deacetylases isozymes sirtuins 1 and 2 (SIRT-1 and SIRT-2) have a complex interplay and both play a role in the rewarding effects of ethanol.

Author Correction: AHR is a Zika virus host factor and a candidate target for antiviral therapy.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

AHR is a Zika virus host factor and a candidate target for antiviral therapy.

Zika virus (ZIKV) is a flavivirus linked to multiple birth defects including microcephaly, known as congenital ZIKV syndrome. The identification of host factors involved in ZIKV replication may guide efficacious therapeutic interventions. In genome-wide transcriptional studies, we found that ZIKV infection triggers aryl hydrocarbon receptor (AHR) activation.

Nrf2/ARE Pathway Modulation by Dietary Energy Regulation in Neurological Disorders.

Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of an array of enzymes with important detoxifying and antioxidant functions. Current findings support the role of high levels of oxidative stress in the pathogenesis of neurological disorders. Given the central role played by Nrf2 in counteracting oxidative damage, a number of studies have targeted the modulation of this transcription factor in order to confer neuroprotection.

Repeated Restraint Stress Decreases Na,K-ATPase Activity via Oxidative and Nitrosative Damage in the Frontal Cortex of Rats.

Chronic psychogenic stress can increase neuronal calcium influx and generate the intracellular accumulation of oxidative (ROS) and nitrosative (RNS) reactive species, disrupting synaptic transmission in the brain. These molecules impair the Na,K-ATPase (NKA) activity, whose malfunction has been related to neuropsychiatric disorders, including anxiety, depression, schizophrenia, and neurodegenerative diseases. In this study, we assessed how 14 days of restraint stress in rats affect NKA activity via oxidative/nitrosative damage in the frontal cortex (FCx), a crucial region for emotional and cognitive control.

Environmental enrichment prevents acute restraint stress-induced anxiety-related behavior but not changes in basolateral amygdala spine density.

Previous studies showed that acute restraint stress or transient elevation of glucocorticoid (GC) stress hormones produces emergent changes in both anxiety behavior and dendritic branches in the basolateral amygdala complex (BLA) of rats. In this work, we demonstrate that exposure to environmental enrichment (EE) prevented stress-induced increases in anxiety (emerging 10 days post-stress) in adult rats without blocking stress-induced dendritic branch remodeling in the BLA nor stress-induced enhancement of GC serum levels.