Correction on: Zhang G, Hu Q and Zou H (2026) Bridging reward and resilience: the endocannabinoid system as a unifying mechanism in exercise-induced protection against major depressive disorder. Front. Psychiatry 17:1766980. doi: 10.3389/fpsyt.2026.1766980.In the published article, several full references were erroneously embedded in the main text, and several in-text citations were not displayed correctly. In addition, one sentence in Section 5.4.2 cited a physical-exercise study while referring to a conventional SSRI antidepressant. The affected passages have been corrected as follows.In the published article, a full reference was erroneously embedded in the first paragraph of the section "2.2 ECS dysfunction: homeostasis failure in depression". A correction has been made to the section 2.2 ECS dysfunction: homeostasis failure in depression, Paragraph 1: "Given the central role of the ECS in sustaining neural homeostasis, its dysfunction is naturally tightly linked to the pathophysiology of depression. Substantial evidence from both preclinical and clinical studies has established that a deficit in endocannabinoid signaling represents a key etiological factor in depression, positioning the pharmacological augmentation of this system as a potential therapeutic target (25,49). A large amount of preclinical and clinical evidence suggests that a depressive state is associated with a broader endocannabinoid deficiency, encompassing not only the classic ligands and CB1 receptors but also dysregulation within the expanded ECS network."The original version of this article has been updated.In the published article, full references were erroneously embedded in the main text of the section "3.1.3 Motor, ECS and neural circuit remodeling". A correction has been made to the section 3.1.3 Motor, ECS and neural circuit remodeling, Paragraph 1: " More significantly, exercise via CB1 receptor-induced effects expand beyond acute neurotransmitter modulation to the long-term neuroplasticity level (22,81). At the synaptic level, activation of CB1 receptors can boost durable functional and structural modifications. A study of long-term depression (iLTD) targeting inhibitory synaptic transmission uncovered that CB1-iLTD relies on protein synthesis and ubiquitination to drive structural modifications that decrease GABA release in the long term (82). This reveals that the exercise-driven eCB-CB1 signaling pathway can persistently promote interneuronal communication and reshape neural circuits by causing protein synthesis-and ubiquitination-dependent presynaptic remodeling. This structural plasticity is fundamental for the brain to adapt to environmental challenges and repair functional deficits. Moreover, the benefits of exercise may be determined by a wider signaling network, the endocannabinoidome (eCBome), which appears to play a significant role in the correlation between exercise and neurological health and may contribute to exercise-driven central and peripheral adaptive mechanisms, thus benefiting mental health (83)."The original version of this article has been updated.In the published article, several full references were erroneously embedded in the main text of the section "3.1.4 potential modulation of extended ECS network through exercise". A correction has been made to the section 3.1.4 potential modulation of extended ECS network through exercise, Paragraph 1:"Although the acute and long-term benefits of exercise are closely related to the regulation of classic endocannabinoid signaling through CB1 and CB2 receptors, additional ECS-associated targets such as GPR55, TRPV1, and PPARγ may also participate in these effects (36 -40, 44). Exercise can increase circulating endocannabinoid levels, including AEA (76), while AEA itself can signal through both CB1-and TRPV1-related pathways depending on concentration and context (38,39). Likewise, PPAR γ provides a plausible mechanistic link between endocannabinoid signaling, metabolism, and inflammatory regulation (40, 44). GPR55 has also been implicated in synaptic plasticity, neurogenesis, and neuroprotection (36, 37). However, direct evidence that exercise specifically modulates GPR55, TRPV1, or PPARγ in depression models remains limited. Therefore, these pathways should presently be considered plausible but incompletely validated extensions of the exercise-ECS axis rather than established mediators."The original version of this article has been updated.In the published article, a full reference was erroneously embedded in the main text of the section "4.2.1 Modulation of exercise via the ECS". A correction has been made to the section 4.2.1 Modulation of exercise via the ECS, Paragraph 1: " Exercise is a powerful physiological activator of the ECS. Cross-species study has determined that exercise-driven eCB signaling is significantly increased in humans and dogs after high-intensity endurance running (76). This finding suggests the evolutionary conservation of the exercise-activated ECS. More systematic evidence comes from a meta-analysis that suggested a coherent-enhancing effect of acute exercise on eCBs: the meta-analysis displayed significant increases in AEA and 2-AG after acute exercise in various patterns species and with or without pre-existing health conditions. The study further reports that the ECS plays a key role in sustaining homeostasis, and that chronic stress may hinder eCB signaling, so exercise as a behavioral intervention targeting the ECS may be a promising treatment for the prevention and treatment of stress-associated disorders (108). Exercise-driven enhanced levels of AEA and 2-AG exert their emotion-regulating and neuroprotective effects by activating extensively distributed CB1 receptors in the brain (76). Through these biological mechanisms, exercise can promote finer emotional regulation and enhance the ability to cope with stress. Via these effects, exercise can systematically enhance the brain ' s tolerance to stress and its ability to recover from stress, thereby significantly decreasing the risk of depression."The original version of this article has been updated.In the published article, a sentence in the section " 5.4.2 Evidence contradictions and measurement limitations of ECS as an intermediary biomarker " contained a citation-text mismatch, because a study on physical exercise after chronic stress was cited while the sentence referred to a conventional SSRI antidepressant. A correction has been made to the section 5.4.2 Evidence contradictions and measurement limitations of ECS as an intermediary biomarker, Paragraph 2: " Furthermore, there is inconsistency in the exercise response. Although studies support that moderate-intensity aerobic exercise can increase peripheral AEA and 2-AG levels (80, 94), other studies have found that the patterns of changes in these molecules after resistance training are different or even opposite. Acute resistance exercise can lead to a significant decrease in peripheral AEA levels (85), and long-term resistance training can also reduce the plasma levels of AEA and 2-AG (88). Additionally, the strength of the correlation between mood improvement and changes in eCBs levels varies greatly across different studies (162), suggesting the presence of underrecognized moderating variables (such as individual genetic background and sampling time points). Direct clinical evidence for the neuroplasticity hypothesis also needs to be strengthened. Although animal models clearly demonstrate that exercise promotes BDNF release and hippocampal neurogenesis through the endocannabinoid system (ECS) (163), and in healthy individuals, a single session of moderate-intensity exercise leads to memory improvement associated with simultaneous increases in anandamide (AEA) and BDNF levels (164), longitudinal clinical studies directly verifying the complete causal chain of 'exercise → ECS activation → BDNF/hippocampal structural changes → symptom relief' in patients with major depressive disorder (MDD) are still relatively scarce."The original version of this article has been updated.
Zhang et al. (Thu,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: