Presentation Title: The Role of Alcohol in Hippocampal Calcium Channel (Cav1.2) expression
Author Name(s): Ryan Kokoska1, Eric Rodriguez2, Bryan Yamamoto2
Author Department and School Affiliation: 1Indiana University School of Medicine; 2Indiana University School of Medicine, Department of Pharmacology and Toxicology
Background and Hypothesis: L-type calcium channels (including Cav1.2) play important roles in hippocampal glutamatergic neurotransmission underlying memory and learning. Their overexpression is implicated in cell death and chronic alcoholism. While increases in hippocampal Cav1.2 gene expression have been reported following chronic involuntary ethanol exposure, the regional distribution has not. We hypothesize that the expression of hippocampal Cav1.2 channels is increased by EtOH drinking in a region-specific manner.
Methods: Male Sprague Dawley rats were allowed 28 days of intermittent-access to 10% EtOH solution. 24 hours after last exposure, brains were collected and processed for immunohistochemistry. Cav1.2-associated immunofluorescent signal from hippocampal subregions was quantified using ImageJ analysis software.
Results: Immunohistochemical results indicate that Cav1.2 immunoreactivity in the hippocampal stratum granulosum layer within the Dentate Gyrus and the stratum pyramidale layer within CA1 and CA3 regions was increased in response to EtOH treatment. There was no significant change for the CA2 region.
Conclusion: This study suggests that calcium signaling in hippocampal subregions is differentially affected by EtOH consumption, which may contribute to calcium-mediated apoptosis.
Impact and Implications: Understanding the process of EtOH-induced hippocampal calcium signaling presents opportunities for understanding the consequences of chronic alcohol exposure related to hippocampal function, and possible interventional therapies.