Interestingly, the opposite effect was seen in females, where optogenetic activation of glutamatergic neurons of the ACC increased formalin-induced nociceptive behavior during conditioning. The abolition of F-CPA following optogenetic inhibition of glutamatergic neurons of the ACC was associated with a reduction in c-Fos immunoreactivity in the ACC in male rats, but not female rats. These results suggest that excitatory glutamatergic neurons of the ACC play differential and sex-dependent roles in the aversion learning and acute sensory components of pain.Depression is a chronic debilitating disorder predicted to affect around 20% of the world population. Both brain and peripheral changes, including neuroplastic changes have been shown to occur in the brains of depressed individuals and animal models of depression. Over the past few decades, growing evidence has supported the role of miRNAs as regulators of critical aspects of brain plasticity and function, namely in the context of depression. These molecules are not only highly expressed in the brain, but are also relatively stable in bodily fluids, including blood. Previous microarray analysis from our group has disclosed molecular players in the hippocampal dentate gyrus (DG), in the context of depression and antidepressant treatment. Two miRNAs in particular-miR-409-5p and miR-411-5p-were significantly up-regulated in the DG of an unpredictable chronic mild stress (CMS) rat model of depression and reversed by antidepressant treatment. Here, we further analyzed the levels of these miRNAs along the DG longitudinal axis and in other brain regions involved in the pathophysiology of depression, as well as in peripheral blood of CMS-exposed rats and after fluoxetine treatment. The effects of CMS and fluoxetine treatment on miR-409-5p and miR-411-5p levels varied across brain regions, and miR-411-5p was significantly decreased in the blood of fluoxetine-treated rats.  https://www.selleckchem.com/products/ins018-055-ism001-055.html  Additional bioinformatic analyses revealed target genes and pathways of these miRNAs related to neurotransmitter signaling and neuroplasticity functions; an implication of the two miRNAs in the regulation of the cellular and molecular changes observed in these brain regions in depression is worth further examination.Subjective values for food rewards guide our dietary choices. There is growing evidence that value signals are constructed in the brain by integrating multiple types of information about flavor, taste, and nutritional attributes of the foods. However, much less is known about the influence of food-extrinsic factors such as labels, brands, prices, and packaging designs. In this mini-review article, we outline recent findings in decision neuroscience, consumer psychology, and food science about the effect of extrinsic factors on food value computations in the human brain. To date, studies have demonstrated that, while the integrated value signal is encoded in the ventromedial prefrontal cortex, information on the extrinsic factors of the food is encoded in diverse brain regions previously implicated in a wide range of functions cognitive control, memory, emotion and reward processing. We suggest that a comprehensive understanding of food valuation requires elucidation of the mechanisms behind integrating extrinsic factors in the brain to compute an overall subjective value signal.Neuroimaging functional connectivity analyses have shown that the negative coupling between the amygdala and cortical regions is linked to better emotion regulation (ER) in experimental task settings. However, less is known about the neural correlates of ER traits or dispositions. The present study aimed to (1) replicate the findings of differential cortico-limbic coupling during resting-state depending on the dispositional use of emotion regulation strategies. Furthermore, the study aimed to (2) extend prior findings by examining whether differences in cortico-limbic coupling during resting-state predict experiential and neuronal ER success in a standard ER task. To this end, N = 107 healthy adults completed the Emotion Regulation Questionnaire (ERQ), underwent an 8-min resting-state fMRI acquisition, and completed a reappraisal task during fMRI. Functional connectivity maps of basolateral and centromedial amygdala nuclei were estimated with a seed-based approach regarding associations with regions of the prefrontal cortex and were then correlated with ERQ scores as well as experiential and neuronal ER success. All hypotheses and the analysis plan are preregistered at https//osf.io/8wsgu. Opposed to prior findings, we were not able to replicate a correlation of dispositional ER strategy use with functional connectivity between the amygdala and PFC regions (p > 0.05, FWE-corrected). Furthermore, there was no association of experiential and neuronal reappraisal success with functional connectivity between amygdala and insula as well as PFC (p > 0.05, FWE-corrected). The present preregistered study calls into question the reported association between individual differences in resting-state cortico-limbic connectivity and dispositional use of ER strategies. However, ongoing advances in functional brain imaging and distributed network approaches may leverage the identification of reliable functional connectivity patterns that underlie successful emotion regulation.Chronic ethanol intake results in brain oxidative stress and neuroinflammation, which have been postulated to perpetuate alcohol intake and to induce alcohol relapse. The present study assessed the mechanisms involved in the inhibition of (i) oxidative stress; (ii) neuroinflammation; and (iii) ethanol intake that follow the administration of the antioxidant N-acetylcysteine (NAC) and the anti-inflammatory acetylsalicylic acid (ASA) to animals that had consumed ethanol chronically. At doses used clinically, NAC [40 mg/kg per day orally (p.o.)] and ASA (15 mg/kg per day p.o.) significantly inhibited chronic alcohol intake and relapse intake in alcohol-preferring rats. The coadministration of both drugs reduced ethanol intake by 65% to 70%. N-acetylcysteine administration (a) induced the Nrf2-ARE system, lowering the hippocampal oxidative stress assessed as the ratio of oxidized glutathione (GSSG)/reduced glutathione (GSH); (b) reduced the neuroinflammation assessed by astrocyte and microglial activation by immunofluorescence; and (c) inhibited chronic and relapse ethanol intake.