[Binge drinking in the young population: Lost memory after initial ethanol exposure via neuroinflammation and epigenetic].

Binge drinking (BD) in young adults/adolescents can lead to cognitive deficits in the adult probably through neuroinflammation and epigenetic. However, the mode of action of alcohol during the initial exposure is less known while it may be the origin of the deficits seen in adults. Recent studies in adolescent rat hippocampus revealed that loss of memory occurred since the very first exposure to BD with similar mechanisms than those highlighted for longer alcohol exposure.

Anti-inflammatory drugs prevent memory and hippocampal plasticity deficits following initial binge-like alcohol exposure in adolescent male rats.

Rationale: Binge drinking during adolescence impairs learning and memory on the long term, and many studies suggest a role of neuroinflammation. However, whether neuroinflammation occurs after the very first exposures to alcohol remains unclear, while initial alcohol exposure impairs learning for several days in male rats.

Objectives: To investigate the role of neuroinflammation in the effects of only two binge-like episodes on learning and on neuronal plasticity in adolescent male rat hippocampus.

Rescuing SLAMF3 Expression Restores Sorafenib Response in Hepatocellular Carcinoma Cells through the Induction of Mesenchymal-to-Epithelial Transition.

Background: Acquired resistance to sorafenib in hepatocellular carcinoma (HCC) patients results in poor prognosis. Epithelial-to-mesenchymal transition (EMT) is the major mechanism implicated in the resistance to sorafenib. We have reported the tumor suppressor role of SLAMF3 (signaling lymphocytic activation molecules family 3) in HCC progression and highlighted its implication in controlling the MRP-1 transporter activity.

Astrogliosis and compensatory neurogenesis after the first ethanol binge drinking-like exposure in the adolescent rat.

Background: Multiple ethanol binge drinking-like exposures during adolescence in the rat induce neuroinflammation, loss of neurogenesis, and cognitive deficits in adulthood. Interestingly, the first ethanol binge drinking-like exposure during adolescence also induces short- term impairments in cognition and synaptic plasticity in the hippocampus though the cellular mechanisms of these effects are unclear. Here, we sought to determine which of the cellular effects of ethanol might play a role in the disturbances in cognition and synaptic plasticity observed in the adolescent male rat after two binge-like ethanol exposures.

Patch-Clamp Recording of Low Frequency Stimulation-induced Long-Term Synaptic Depression in Rat Hippocampus Slices During Early and Late Neurodevelopment.

Background: Studying synaptic plasticity in the rat hippocampus slice is a well-established way to analyze cellular mechanisms related to learning and memory. Different modes of recording can be used, such as extracellular field excitatory post-synaptic potential (EPSP) and diverse patch-clamp methods. However, most studies using these methods have examined only up to the juvenile stage of brain maturation, which is known to terminate during late adolescence/early adulthood.