Decreased kynurenine pathway potentiate resilience to social defeat effect on cocaine reward

Giménez-Gómez, Pablo; Ballestín, Raúl; Biedma-Elduayen, Leticia Gil de; Vidal, Rebeca; Ferrer-Pérez, Carmen; Reguilón, Marina D.; O’Shea, Esther; Miñarro, José; Colado, María Isabel; Rodrı́guez-Arias, Marta

doi:10.1016/j.neuropharm.2021.108753

Cited by 14 publications

(10 citation statements)

References 127 publications

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“…Male mice in the regular housing condition were housed in groups of four in transparent plastic cages (27 × 27 × 14 cm) with no more enrichment than standard bedding (wood flakes 1–3.35 mm), nesting material (paper strands) and two wooden gnaw sticks (5 x 1 × 1 cm) per cage. Male mice in EE conditions were housed in groups of four in plastic cages (59 x 38 × 20 cm) with standard bedding and nesting material, two wooden gnaw sticks plus additional PVC tunnel (13 × 5.5 cm) and a plastic mouse house (12.5 x 10.5 × 11 cm; Ferrer-Pérez, 2019 ; Giménez-Gómez et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

“…To further characterize the potentiation of the resilience response, a second experiment took place to evaluate the effect of environmental enrichment (EE) exposure during adolescence, prior to the SD stress. The EE model selected for this work can be considered a basic and modest EE model, which based on the results obtained previously ( Giménez-Gómez et al, 2021 ), we hypothesize is sufficient to stimulate resilience and block the increase in the reinforcing effects of ethanol and the neuroinflammatory response induced by SD.…”

Section: Introductionmentioning

confidence: 99%

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Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience

Reguilón

Ferrer-Pérez

Manzanedo

et al. 2021

Neurobiology of Stress

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience

Reguilón

Ferrer-Pérez

Manzanedo

et al. 2021

Neurobiology of Stress

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“…Abnormal apoptosis has been observed in the brain areas closely associated with emotion and cognition, including the hippocampus, the amygdala, and the medial PFC in single prolonged stress model of PTSD [ 333 ]. In addition, the decreased kynurenine pathway potentiates resilience to the social defeat effect of a cocaine reward [ 334 ]. Early intervention with a glucocorticoid receptor antagonist a RU486 facilitates the correction of traumatic stress-induced fear and anxiety dysregulation [ 335 ].…”

Section: Diseases Linked To Mitochondrial Dysfunctionmentioning

confidence: 99%

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan–Kynurenine Metabolic System

Tanaka

Szabó

Spekker

et al. 2022

Cells

125

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Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mitochondrial functions has been probed in the pathogenesis of a wide range of illnesses including neurodegenerative diseases. Recently, a growing number of preclinical studies have revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular signaling, and gene expression, among others. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)–kynurenine (KYN) metabolic system, which observably contributes to the development of pathological conditions including neurological and psychiatric disorders. This review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.

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Section: Post-traumatic Stress Disordermentioning

confidence: 99%

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan-Kynurenine Metabolic System

Tanaka¹,

Szabó²,

Spekker³

et al. 2022

Preprint

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Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mitochondrial functions has been probed in the pathogenesis of a wide range of illnesses including neurodegenerative diseases. Recently growing number of preclinical studies has revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular signaling, and gene expression, among other. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)-kynurenine (KYN) metabolic system, which observably contributes to development of pathological conditions including neurological and psychiatric disorders. This narrative review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.

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Decreased kynurenine pathway potentiate resilience to social defeat effect on cocaine reward

Cited by 14 publications

References 127 publications

Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience

Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan–Kynurenine Metabolic System

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan-Kynurenine Metabolic System

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