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Low food availability caused higher concentrations of fecal corticosterone metabolites, as well as higher liver and lower spleen weights, suggesting an adaptation of the metabolism to this situation.After ten 5-min sessions of access to 32% sucrose, a reward downshift (RD) to 2% sucrose induces a transient rejection of the reward. Animals were segregated according to the speed of recovery from RD into Fast-recovery and Slow-recovery subgroups. Animals were subsequently trained in an operant licking (OL) task in which licking at an empty tube provided 10 s of access to a second tube containing 66% alcohol. Licking on the first tube was subjected to a progressive ratio (PR) schedule with a step of 4 licks. Fast-recovery animals (both males and females) licked to a higher ratio than Slow-recovery animals. Animals were also exposed to a well-lit open field (OF) for 20 min. Fast- and Slow-recovery males and females exhibited equal levels of activity in the OF. Tissue samples from tails were assessed for two well-known allelic variations of the human opioid receptor gene, OPRM1, known to affect mu opioid sensitivity The C17T and A118G single nucleotide polymorphisms. There was no evidence of a relationship between genotype and behavior, suggesting that these genetic mechanisms in humans do not account for the individual differences in recovery from RD and OL for alcohol in rats.Binge eating disorder (BED), characterized by excessive food consumption within a discrete period of time, is the most prevalent of all eating disorders, with higher rates in women than men. Chronic stress, particularly during adolescence, is a significant risk factor for BED in women, but the mechanism underlying this relationship remains elusive. We investigated the phenomenon by testing the impact of mid-adolescent intermittent physical stress (IPS) on binge-like intake of sucrose in adult female rats, assessing how the behavior changed across reproductive cycles. One hundred and nineteen Long-Evans rats were exposed to IPS (n = 59) or no stress (NS; n = 60) for 12 days during mid-adolescence (PD35-46). Binge-like eating was induced in adult animals using an intermittent access protocol animals were provided with 12 h or 24 h access to sucrose, 12 h access to saccharin, or 12 h access to food over 28 days. After 1- or 28-day abstinence, compulsive responding for sucrose was measured using a conditioned suppression paradigm. GLPG0634 chemical structure Rats given 12 h access to sucrose developed binge-like intake, measured as increased consumption during the first hour; the effect was magnified in IPS animals and most pronounced during proestrous. Solution intake in IPS rats was predicted by open arm entries in the elevated plus maze, suggesting that increased risk-taking behavior is associated with greater binge-like eating. IPS blocked conditioned suppression after 28 days of abstinence, pointing to a role of mid-adolescent stress in compulsivity. Collectively, these findings emphasize the impact of stress on the emergence of binge eating in females and suggest that intervention programs for women with a history of adolescent adversity should be investigated as a means to reduce risk for BED.Compared to the field of anxiety research, the use of fear conditioning paradigms for studying chronic pain is relatively novel. Developments in identifying the neural correlates of pain-related fear are important for understanding the mechanisms underlying chronic pain and warrant synthesis to establish the state-of-the-art. Using effect-size signed differential mapping, this meta-analysis combined nine MRI studies and compared the overlap in these correlates of pain-related fear to those of other non-pain-related conditioned fears (55 studies). Pain-related fear was characterized by neural activation of the supramarginal gyrus, middle temporal gyrus, inferior/middle frontal gyri, frontal operculum and insula, pre-/post-central gyri, medial frontal and (para-)cingulate cortex, hippocampus, thalamus, and putamen. There were differences with other non-pain-related conditioned fears, specifically in the inferior frontal gyrus, medial superior frontal gyrus, post-central gyrus, middle temporal gyrus, parieto-occipital sulcus, and striatum. We conclude that pain-related and non-pain-related conditioned fears recruit overlapping but distinguishable networks, with potential implications for understanding the mechanisms underlying different psychopathologies.The fluted giant clam, Tridacna squamosa, can perform light-enhanced shell formation, aided by its symbiotic dinoflagellates (Symbiodinium, Cladocopium, Durusdinium), which are able to donate organic nutrients to the host. During light-enhanced shell formation, increased Ca2+ transport from the hemolymph through the shell-facing epithelium of the inner mantle to the extrapallial fluid, where calcification occurs, is necessary. Additionally, there must be increased absorption of exogenous Ca2+ from the surrounding seawater, across the epithelial cells of the ctenidium (gill) into the hemolymph, to supply sufficient Ca2+ for light-enhanced shell formation. When Ca2+ moves across these epithelial cells, the low intracellular Ca2+ concentration must be maintained. Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) regulates the intracellular Ca2+ concentration by pumping Ca2+ into the sarcoplasmic/endoplasmic reticulum (SR/ER) and Golgi apparatus. Indeed, the ctenidium and inner mantle of T. squamosa, expressed a homolog of SERCA (SERCA-like transporter) that consists of 3009 bp, encoding 1002 amino acids of 110.6 kDa. SERCA-like-immunolabeling was non-uniform in the cytoplasm of epithelial cells of ctenidial filaments, and that of the shell-facing epithelial cells of the inner mantle. Importantly, the protein abundance of SERCA-like increased significantly in the ctenidium and the inner mantle of T. squamosa after 12 h and 6 h, respectively, of light exposure. This would increase the capacity of pumping Ca2+ into the endoplasmic reticulum and avert a possible surge in the cytosolic Ca2+ concentration in epithelial cells of the ctenidial filaments during light-enhanced Ca2+ absorption, and in cells of the shell-facing epithelium of the inner mantle during light-enhanced shell formation.