![]() ![]() It remains unclear which factors provide resilience to stress in certain individuals and what are the underlying mechanisms ( Larrieu and Sandi, 2018 Ménard et al., 2017). However, not all individuals are equally affected by stress ( Duclot and Kabbaj, 2013 McEwen et al., 2015 Russo et al., 2012) while some individuals show a high vulnerability to develop depression, others endure resilience following stress exposure ( Russo et al., 2012 Weger and Sandi, 2018). Mitochondria, by powering the brain with energy production, play a central role in the adaptation and response to stress ( Picard et al., 2015), and mitochondrial supplements could provide an efficient means of protecting brain structures that are particularly vulnerable to stress ( Parikh et al., 2009). Accordingly, stress-associated depletion of brain's energy resources could lead to impaired neuronal plasticity underlying depression ( Morava and Kozicz, 2013 Picard et al., 2018). In addition, chronic stress has a strong capacity to trigger and exacerbate depression ( de Kloet et al., 2005 Richter-Levin and Xu, 2018) and impinges metabolic-costly neuronal adaptations in structure and function ( Turner and Lloyd, 2004 de Kloet et al., 2005 McEwen et al., 2015). The strong reliance of the brain on high energy consumption would make it particularly vulnerable to metabolic alterations ( Pei and Wallace, 2018). Metabolic alterations are emerging as key etiological factors for the development of neuropsychiatric disorders, including depression ( Pei and Wallace, 2018 Andreazza and Nierenberg, 2018 Kim et al., 2019). ![]() Introductionĭepression is among the leading causes of disability worldwide, which reflects the current lack of understanding of its underlying mechanisms ( Friedrich, 2017 Menke, 2018). Therefore, we reveal a metabolic signature in the NAc for antidepressant-like effects of LAC in vulnerable mice characterized by restoration of stress-induced neuroenergetics alterations and lipid function. High rank mice also showed reduced levels of several energy-related metabolites in the NAc that were counteracted by LAC treatment. High rank, but not low rank, mice, as assessed with the tube test, showed behavioral vulnerability to stress, supporting a higher susceptibility of high social rank mice to develop depressive-like behaviors. We investigated the metabolic impact in the NAc of antidepressant LAC treatment in chronically-stressed mice using 1H-magnetic resonance spectroscopy ( 1H-MRS). Acetyl-L-carnitine (LAC), a mitochondria-boosting supplement, has shown promising antidepressant-like effects opening therapeutic opportunities for restoring energy balance in depressed patients. Energy metabolic changes in the nucleus accumbens (NAc) were recently related to hierarchical status and vulnerability to develop depression-like behavior. ![]() ![]() Emerging evidence suggests that hierarchical status provides vulnerability to develop stress-induced depression. ![]()
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