Taken together, decreased of CACNA1C mRNA in these animals [ 25 ], together with increased protein expression in the present study, the identification of L-type Ca channel blockers as a predicted therapeutic target [ 25 ], as well as the increased CACNA1C mRNA in human subjects with AUD in the present study and the prior report of increased CACNA1C mRNA and protein in the hippocampus of rats with chronic alcohol exposure [ 6 ] reveal a strong trend for increased CACNA1C hippocampal expression with chronic alcohol exposure and highlight the importance of cross species comparisons and multiple outcome measures.
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Cross-Species evidence for hippocampal CACNA1C as a therapeutic target for alcohol use disorder.
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