Topic: Binge drinking

Alcohol raises concerns due to the episodic and intense alcohol intake observed in adolescents. Recent studies reveal a correlation between escalated EtOH intake and neuroinflammation, emphasizing the endocannabinoid (eCB) system´s engagement. Our previous data in mice revealed that intermittent EtOH-exposure during adolescence leads to elevated levels of the ω-6 arachidonic acid (AA) in adulthood. AA is intricately linked to the neuroinflammatory response as a precursor of proinflammatory prostaglandins, and its brain levels are intertwined with balance between the synthesis and hydrolysis of

Binge drinking (BD) is characterized by consuming at least 70 g for men and 56 g for women of pure alcohol within two hours. Clinical studies examining the impact of BD on memory in young adults have revealed impairments across various types of memory (episodic, visuospatial, working memory...), although the frequency of BD often varies among studies. Preclinical research indicates that BD leads to the degradation of glutamate-dependent synaptic plasticity, the cellular mechanism of learning and memory in the hippocampus, including the metabotropic form of glutamatergic long-term synaptic depr

Binge drinking (BD) consists in high and rapid episodes of ethanol consumption interspaced with abstinence. Studies in adolescent rats showed that history of BD during this period of brain maturation impair memory on the long-term. However, the mechanisms of these effects remain unclear. Others and we found that pre-treatment with minocycline, an antibiotic with anti-inflammatory properties prevented some of the negative effects of BD on hippocampus long-term synaptic depression (LTD) and learning behaviour. However, whether NMDA- and mGlu-LTD are similarly affected, and which of these forms o