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The prelimbic cortex and amygdala regulate the extinction of conditioned fear and anxiety, respectively. In adult rats, chronic stress affects the dendritic morphology of these brain areas, slowing extinction of learned fear and enhancing anxiety. The aim of this study was to determine whether rats subjected to chronic stress in adolescence show changes in learned fear, anxiety, and synaptic transmission in the prelimbic cortex during adulthood. Male Sprague Dawley rats were subjected to seven days of restraint stress on postnatal day forty-two (PND 42, adolescence). Afterward, the fear-conditioning paradigm was used to study conditioned fear extinction. Anxiety-like behavior was measured one day (PND 50) and twenty-one days (PND 70, adulthood) after stress using the elevated-plus maze and dark-light box tests, respectively. With another set of rats, excitatory synaptic transmission was analyzed with slices of the prelimbic cortex. Rats that had been stressed during adolescence and adulthood had higher anxiety-like behavior levels than did controls, while stress-induced slowing of learned fear extinction in adolescence was reversed during adulthood. As well, the field excitatory postsynaptic potentials of stressed adolescent rats had significantly lower amplitudes than those of controls, although the amplitudes were higher in adulthood. Our results demonstrate that short-term stress in adolescence induces strong effects on excitatory synaptic transmission in the prelimbic cortex and extinction of learned fear, where the effect of stress on anxiety is more persistent than on the extinction of learned fear. These data contribute to the understanding of stress neurobiology., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Many diseases and degenerative processes affecting the nervous system and peripheral organs trigger the activation of inflammatory cascades. Inflammation can be triggered by different environmental conditions or risk factors, including drug and food addiction, stress, and aging, among others. Several pieces of evidence show that the modern lifestyle and, more recently, the confinement associated with the COVID-19 pandemic have contributed to increasing the incidence of addictive and neuropsychiatric disorders, plus cardiometabolic diseases. Here, we gather evidence on how some of these risk factors are implicated in activating central and peripheral inflammation contributing to some neuropathologies and behaviors associated with poor health. We discuss the current understanding of the cellular and molecular mechanisms involved in the generation of inflammation and how these processes occur in different cells and tissues to promote ill health and diseases. Concomitantly, we discuss how some pathology-associated and addictive behaviors contribute to worsening these inflammation mechanisms, leading to a vicious cycle that promotes disease progression. Finally, we list some drugs targeting inflammation-related pathways that may have beneficial effects on the pathological processes associated with addictive, mental, and cardiometabolic illnesses. [ABSTRACT FROM AUTHOR]

Confinement during the COVID-19 pandemic has significantly impacted lifestyles worldwide. The aim of this study was to evaluate the effect of confinement on anxiety symptoms and sleep quality in people living in extreme southern latitudes. The Beck Anxiety Inventory (BAI) and the Pittsburgh Sleep Quality Index (PSQI) were administered to 617 people, 74.2% of whom were women. The sample was grouped according to confinement: the zone of confinement (CZ) (46.5%) and the zone of partial confinement (PZ) (53.5%). In addition, the sample was further categorized into four age subgroups (18–25 years; 26–40 years; 41–50 years; over 50 years). Higher levels of anxiety and worse sleep quality were found in the CZ group than in the PZ group. Women had higher levels of anxiety and worse sleep quality than men. A significant bidirectional relationship between anxiety and sleep quality was observed, even after controlling for sex. This study demonstrated that women and young adults were more vulnerable to the effects of confinement on anxiety symptoms and sleep quality in populations at southern latitudes. [ABSTRACT FROM AUTHOR]

Chronic stress leads to secretion of the adrenal steroid hormone corticosterone, inducing hippocampal atrophy and dendritic hypertrophy in the rat amygdala. Both alterations have been correlated with memory impairment and increased anxiety. Supplementation with w-3 fatty acids improves memory and learning in rats. The aim of this study was to evaluate the effects of w-3 supplementation on learning and major biological and behavioral stress markers. Male Sprague-Dawley rats were randomly assigned to three experimental groups: 1) Control, 2) Vehicle, animals supplemented with water, and 3) w-3, rats supplemented with ?-3 (100 mg of DHA+25 mg of EPA). Each experimental group was divided into two subgroups: one of which was not subjected to stress while the other was subjected to a restraint stress paradigm. Afterwards, learning was analyzed by avoidance conditioning. As well, plasma corticosterone levels and anxiety were evaluated as stress markers, respectively by ELISA and the plus-maze test. Restraint stress impaired learning and increased both corticosterone levels and the number of entries into the open-arm (elevated plus-maze). These alterations were prevented by w-3 supplementation. Thus, our results demonstrate that w-3 supplementation had two beneficial effects on the stressed rats, a strong anti-stress effect and improved learning. [ABSTRACT FROM AUTHOR]