The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 17 No. 9 • October 2014

Rapid Antidepressant Effects Elicited By
L-Acetylcarnitine Treatment in Rats and Mice

Another example of a recent discovery of genetic expression modified by epigenetic mechanisms was reported in a recent paper.7 In this study, rats with a genetic defect that results in reduced expression of certain glutamate receptors (mGlu2/3) and a spontaneous depressive state were treated with L-acetylcarnitine, a natural acetylating agent with antidepressant, antianxiety, and anti-pain effects (gene expression is modified by the addition of an acetyl group to DNA in certain brain regions). The activation of mGlu2/3 glutamate receptors shortens the time required for the therapeutic efficacy of conventional antidepressants in rats with this genetic defect. The results showed that treatment with L-acetylcarnitine, a naturally occurring molecule, caused a “rapid, robust, and long-lasting antidepressant effect” in the genetic model of depression in rats as well as (another part of the same study) the depression induced in mice by chronic unpredictable stress. Antidepressive effects were assessed by sucrose preference (depressed rodents ingest less sucrose) and the forced swim test, but the treatment also resulted in correction of the reduced BDNF (brain derived neurotrophic factor) in the hypothalamus of the rats with the genetic defect.


7. Nasca, Xenos, Barone et al. L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors. Proc Natl Acad Sci U S A. 110(12):4804-9 (2013).

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