Repetitive binge-like consumption based on the Drinking-in-the-Dark model alters the microglial population in the mouse hippocampus.

Alcoholism causes various maladaptations in the central nervous system, including the neuroimmune system. Studies of alcohol-induced dysregulation of the neuroimmune system generally focus on alcohol dependence and brain damage, but our previous research indicates that repetitive binge-like consumption perturbs cytokines independent of cell death. This paper extends that research by examining the impact of binge-like consumption on microglia in the hippocampus and the amygdala.

A comparison of hippocampal microglial responses in aged and young rodents following dependent and non-dependent binge drinking.

Alcoholism is a highly visible and prevalent issue in the United States. Although binge-drinking is assumed to be a college-age problem, older adults (ages 65+) consume binge amounts of alcohol and have alcohol use disorders (AUDs). Moreover, individuals with alcohol dependence in their youth often continue to drink as they age.

Characterization of the Hippocampal Neuroimmune Response to Binge-Like Ethanol Consumption in the Drinking in the Dark Model.

Objectives: Alcohol dependence leads to dysregulation of the neuroimmune system, but the effects of excessive alcohol consumption on key players of the neuroimmune response after episodic binge drinking in nondependence has not been readily assessed. These studies seek to determine how the neuroimmune system within the hippocampus responds to binge-like consumption prior to dependence or evidence of brain damage.

Methods: C57BL/6J mice underwent the drinking in the dark (DID) paradigm to recapitulate binge consumption.