ht © 2020 Pützer, Brüne, Hatt and Wolf.Problematic alcohol drinking and alcohol dependence are an increasing health problem worldwide. Alcohol abuse is responsible for approximately 5% of the total deaths in the world, but addictive consumption of it has a substantial impact on neurological and memory disabilities throughout the population. One of the better-studied brain areas involved in cognitive functions is the hippocampus, which is also an essential brain region targeted by ethanol. Accumulated evidence in several rodent models has shown that ethanol treatment produces cognitive impairment in hippocampal-dependent tasks. These adverse effects may be related to the fact that ethanol impairs the cellular and synaptic plasticity mechanisms, including adverse changes in neuronal morphology, spine architecture, neuronal communication, and finally an increase in neuronal death. There is evidence that the damage that occurs in the different brain structures is varied according to the stage of development during which the subjects are exposed to ethanol, and even much earlier exposure to it would cause damage in the adult stage. Studies on the cellular and cognitive deficiencies produced by alcohol in the brain are needed in order to search for new strategies to reduce alcohol neuronal toxicity and to understand its consequences on memory and cognitive performance with emphasis on the crucial stages of development, including prenatal events to adulthood. Copyright © 2020 Mira, Lira, Tapia-Rojas, Rebolledo, Quintanilla and Cerpa.Traumatic brain injury (TBI) in various forms affects millions in the United States annually. There are currently no FDA-approved therapies for acute injury or the chronic comorbidities associated with TBI. Acute phases of TBI are characterized by profound neuroinflammation, a process that stimulates the generation and release of proinflammatory cytokines including interleukin-1α (IL-1α) and IL-1β. Both forms of IL-1 initiate signaling by binding with IL-1 receptor type 1 (IL-1R1), a receptor with a natural, endogenous antagonist dubbed IL-1 receptor antagonist (IL-1Ra). The recombinant form of IL-1Ra has gained FDA approval for inflammatory conditions such as rheumatoid arthritis, prompting interest in repurposing these pharmacotherapies for other inflammatory diseases/injury states including TBI. This review summarizes the currently available preclinical and clinical literature regarding the therapeutic potential of inhibiting IL-1-mediated signaling in the context of TBI. Additionally, we propose specific research areas that would provide a greater understanding of the role of IL-1 signaling in TBI and how these data may be beneficial for the development of IL-1-targeted therapies, ushering in the first FDA-approved pharmacotherapy for acute TBI. Copyright © 2020 Thome, Reeder, Collins, Gopalan and Robson.Anxiety disorders (AD) comprise a broad range of psychiatric conditions, including general anxiety (GAD) and specific phobias. For the last decades, the use of animal models of anxiety has offered important insights into the understanding of the association between these psychopathologies. Here, we investigate whether Carioca high- and low-conditioned freezing rats (CHF and CLF, respectively), a GAD animal model of anxiety, show similar high- and low-freezing behavioral phenotypes for cued auditory fear conditioning. Adult CHF (n = 16), CLF (n = 16) and normal age-matched Wistar rats (control, CTL, n = 16) were tested in a classical auditory-cued fear conditioning paradigm over 3 days (Tone + Shock and Tone only groups, n = 8 per treatment). Freezing responses were measured and used as evidence of fear conditioning. CBR-470-1 solubility dmso Overall, both CHF and CLF rats, as well as CTL animals displayed fear conditioning to the auditory CS. However, CLF animals showed a rapid extinction to the auditory conditioned stimulus compared to CHF and CTL rats. We discuss these findings in the context of the behavioral and neuronal differences observed in rodent lines of high and low anxiety traits. Copyright © 2020 Macêdo-Souza, Maisonnette, Filgueiras, Landeira-Fernandez and Krahe.Previous studies suggested that both maladaptive stress response and circadian dysregulation might have a role in the background of migraine. However, effects of circadian genes on migraine have not been tested yet. In the present study, we investigated the main effect of rs10462028 of the circadian locomotor output cycles kaput (CLOCK) gene and its interaction with different stress factors on migraine. In our cross-sectional study 2,157 subjects recruited from Manchester and Budapest completed the ID-Migraine questionnaire to detect migraine type headaches (migraineID). Additional stress factors were assessed by a shortened version of the Childhood Trauma Questionnaire, the List of Threatening Experiences questionnaire, and a validated questionnaire to identify financial difficulties. Rs10462028 showed no main genetic effect on migraineID. However, chronic stress indexed by financial difficulties showed a significant interaction effect with rs10462028 (p = 0.006 in recessive model) on migraineID. This result remained significant after correction for lifetime bipolar and unipolar depression and was replicated in both subsamples, although only a trend effect was reached after Bonferroni-correction, which is the strictest correction not considering interdependences. Childhood adversity (CHA) and Recent negative life events (RLE) showed no significant gene × stress interaction with rs10462028. In addition, in silico analysis demonstrated that the genetic region tagged by rs10462028 alters the binding of several miRNAs. Our exploratory study suggests that variations in the CLOCK gene, with moderating effect on gene function through miRNA binding, in interaction with financial difficulties might influence the risk of migraine-type headaches. Thus, financial hardship as a chronic stress factor may affect migraine through altering circadian rhythms. Copyright © 2020 Baksa, Gonda, Eszlari, Petschner, Acs, Kalmar, Deakin, Bagdy and Juhasz.Objective Patients undergoing major surgeries may experience certain cognitive decline, which is known as postoperative delirium (POD) or postoperative cognitive dysfunction (POCD). We employed integrated behavioral Z-scoring introduced by Guilloux et al. (2011) to investigate the effects of fracture fixation under anesthesia on hippocampus-dependent memory in mice. Methods ICR mice (12-14 months) underwent stabilized tibial fracture operation under sevoflurane anesthesia. They were subjected to a battery of successive hippocampus-dependent tests following surgery, including open field test (OF), novel object recognition (NOR), fear conditioning test (FC), and Morris water maze (MWM). The integrated behavioral Z-scoring was applied to assess the hippocampus-dependent memory after anesthesia/surgery, and the association between the integrated behavioral Z-scores and hippocampal pro-inflammatory cytokines was explored. Results Mice after anesthesia/surgery were found to have impaired hippocampus-dependent memory in NOR, FC, and MWM but with different degrees in these aspects as represented by P-value and effect size.