Physical exercise stimulates hippocampal mTORC1 and FNDC5/irisin signaling pathway in mice: Possible implication for its antidepressant effect

Gruhn, Karen; Siteneski, Aline; Camargo, Anderson; Freitas, Andiara E.; Brocardo, Patrícia S.; Rodrigues, Ana Lúcia S.

doi:10.1016/j.bbr.2020.113040

Cited by 13 publications

(8 citation statements)

References 58 publications

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“…Irisin, which is considered as a mediator of physical activity, has been extensively studied in recent years. In many studies, it was concluded that irisin levels increased with exercise (32)(33)(34)(35)(36). Physical activity has beneficial effects on brain health and cognitive functions.…”

Section: Discussionmentioning

confidence: 99%

Effect of irisin on the epilepsy induced by penicillin G: An electrophysiological study

YILDIZ¹,

DEMİR²,

Beyazçiçek³

et al. 2022

J Exp Clin Med

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Epilepsy is a neurological disease characterized by sudden and synchronized seizures caused by abnormal and excessive electrical discharges in brain neurons. The purpose of this study was to electrophysiologically examine the effects of acute administration of irisin, which is thought to be neuroprotective and increase cell proliferation, at different doses (10 and 100 nM) on the penicillin-induced experimental epilepsy in rats. Fortynine adult male Wistar rats were used in the study. The rats were divided into 7 groups: sham, control group (penicillin), irisin group, the pre-and during-seizure groups of 10 nM and 100 nM irisin. All the substances except penicillin were administered intraperitoneally. The rats were anesthetized using urethane. The bone tissue on the left cerebral cortex was removed and the electrodes were placed in the somatomotor cortex. Thirty minutes before penicillin administration, irisin was administered to the pre-seizure penicillin group at doses of 10 nM and 100 nM. Then, penicillin (500 IU/2 µl) was injected intracortically, and ECoG recording was continued for 120 minutes. On the other hand, 10 nM and 100 nM of irisin were administered to the during-seizure penicillin group after penicillin was injected intracortically and the seizure occurred, and ECoG recording was continued for 120 minutes. The ECoG recordings were analyzed using the PowerLab Chart v.8 software. In conclusion, it was found that irisin prolonged the latency of initial epileptic activity and decreased the number and amplitude of spike-waves in the penicillin-induced experimental epilepsy model. These results suggest that irisin might have an antiepileptic potential.

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Section: Discussionmentioning

confidence: 99%

Effect of irisin on the epilepsy induced by penicillin G: An electrophysiological study

YILDIZ¹,

DEMİR²,

Beyazçiçek³

et al. 2022

J Exp Clin Med

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“…Physical exercise is known to possess antidepressant effects both in humans and rodents [87][88][89][90][91]. The mechanisms underlying its antidepressant effects have been extensively studied and are thought to involve neurogenic stimulation by increasing the expression of brain-derived neurotrophic factor (BDNF) in critical brain regions, particularly in the dentate gyrus of the hippocampus [89,92].…”

Section: Inhibition Of Nlrp3 Inflammasome By Physical Exercisementioning

confidence: 99%

“…Numerous studies have also demonstrated the antidepressant-like effects of physical exercise in rodents [90][91][92]94], while recent reports have also shown that physical activity can inhibit NLRP3 activation in the hippocampus [89,95]. For example, in a study by Wang et al (2016) exercise was shown to attenuate the occurrence of depressive-like behaviors in ovariectomized female rats, while also decreasing hippocampal levels of IL-1β and IL-18 via suppression of NLRP3 inflammasome activation [94].…”

Section: Inhibition Of Nlrp3 Inflammasome By Physical Exercisementioning

confidence: 99%

NLRP3 Inflammasome: From Pathophysiology to Therapeutic Target in Major Depressive Disorder

Kouba

Gil-Mohapel

Rodrigues

2022

IJMS

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Major depressive disorder (MDD) is a highly prevalent psychiatric disorder, whose pathophysiology has been linked to the neuroinflammatory process. The increased activity of the Nod-like receptor pyrin containing protein 3 (NLRP3) inflammasome, an intracellular multiprotein complex, is intrinsically implicated in neuroinflammation by promoting the maturation and release of proinflammatory cytokines such as interleukin (IL)-1β and IL-18. Interestingly, individuals suffering from MDD have higher expression of NLRP3 inflammasome components and proinflammatory cytokines when compared to healthy individuals. In part, intense activation of the inflammasome may be related to autophagic impairment. Noteworthy, some conventional antidepressants induce autophagy, resulting in less activation of the NLRP3 inflammasome. In addition, the fast-acting antidepressant ketamine, some bioactive compounds and physical exercise have also been shown to have anti-inflammatory properties via inflammasome inhibition. Therefore, it is suggested that modulation of inflammasome-driven pathways may have an antidepressant effect. Here, we review the role of the NLRP3 inflammasome in the pathogenesis of MDD, highlighting that pathways related to its priming and activation are potential therapeutic targets for the treatment of MDD.

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“…Moreover, peripheral delivery of FNDC5 also induces hippocampal BDNF expression [ 12 ]. Indeed, exercise-induced FNDC5 and its cleavage product irisin are effective in rescuing neural plasticity deficits in AD mouse models [ 46 ] and depression models [ 47–49 ].…”

Section: Exercise-induced Factors and Neural Plasticitymentioning

confidence: 99%

Exercise and Dietary Factors Mediate Neural Plasticity Through Modulation of BDNF Signaling

Fakhoury

Eid

Ahmad

et al. 2022

BPL

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The term “neural plasticity” was first used to describe non-pathological changes in neuronal structure. Today, it is generally accepted that the brain is a dynamic system whose morphology and function is influenced by a variety of factors including stress, diet, and exercise. Neural plasticity involves learning and memory, the synthesis of new neurons, the repair of damaged connections, and several other compensatory mechanisms. It is altered in neurodegenerative disorders and following damage to the central or peripheral nervous system. Understanding the mechanisms that regulate neural plasticity in both healthy and diseased states is of significant importance to promote cognition and develop rehabilitation techniques for functional recovery after injury. In this minireview, we will discuss the mechanisms by which environmental factors promote neural plasticity with a focus on exercise- and diet-induced factors. We will highlight the known circulatory factors that are released in response to exercise and discuss how all factors activate pathways that converge in part on the activation of BDNF signaling. We propose to harness the therapeutic potential of exercise by using BDNF as a biomarker to identify novel endogenous factors that promote neural plasticity. We also discuss the importance of combining exercise factors with dietary factors to develop a lifestyle pill for patients afflicted by CNS disorders.

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Physical exercise stimulates hippocampal mTORC1 and FNDC5/irisin signaling pathway in mice: Possible implication for its antidepressant effect

Cited by 13 publications

References 58 publications

Effect of irisin on the epilepsy induced by penicillin G: An electrophysiological study

Effect of irisin on the epilepsy induced by penicillin G: An electrophysiological study

NLRP3 Inflammasome: From Pathophysiology to Therapeutic Target in Major Depressive Disorder

Exercise and Dietary Factors Mediate Neural Plasticity Through Modulation of BDNF Signaling

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