Investigating the Role of Astrocytic Calcium Fluxes in Adolescent Intermittent Ethanol-Induced Behavioral Deficits (2016)

Undergraduates: James Andrews, Dr. Donita Robinson, Dr. Ken McCarthy, Dr. Aric Madayag

Faculty Advisor: Donita Robinson
Department: Biology

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Alcohol is the predominant substance of abuse among adolescents in America (NIAAA, 2013). This study sought to determine if astrocytes, the most abundant cell type in the brain (Panchision 2011), modulate the neurobehavioral consequences of adolescent binge drinking (ABD) using a preclinical mouse model of binge drinking previously shown to induce neurobehavioral deficits in adult mice (Coleman et al, 2014), adolescent intermittent ethanol (AIE). Astrocytes are vital to proper neuronal signaling (Squire et al, 2003). In astrocytes, the protein IP3R2 regulates Ca2+ fluxes, a signal of cellular excitation. Little is known about whether or not astrocytes contribute to the neuropathology of AIE. We hypothesized that silencing evoked astrocytic Ca2+ fluxes would diminish AIE-induced behavioral deficits in adulthood by altering proper neuronal signaling. Wild-type (floxed) mice and IP3R2 conditional knockout mice were treated with AIE or water and tested for working memory and reversal learning in an attentional set-shifting paradigm as well as locomotion in a novel open field. Results show no interaction between IP3R2 and AIE treatment, suggesting astrocytic Ca2+ fluxes can be discounted as a regulator of AIE-induced working memory, reversal learning, or locomotive deficits. Astrocytic Ca2+ fluxes are poor targets for treating the pathological consequences of ABD. Future studies may investigate the role of other astrocytic signaling pathways, such as the cAMP-dependent pathway.