Long term adequate n-3 polyunsaturated fatty acid diet protects from depressive-like behavior but not from working memory disruption and brain cytokine expression in aged mice

Moranis, Aurélie; Delpech, Jean-Christophe; Smedt-Peyrusse, Véronique de; Aubert, Agnès; Guesnet, Philippe; Lavialle, Monique; Joffre, Corinne; Layé, Sophie

doi:10.1016/j.bbi.2011.11.001

Cited by 88 publications

(80 citation statements)

References 93 publications

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“…Pellets were prepared by UPAE-Institut national de la recherche agronomique and stored at 4°C. Fatty acid composition was regularly controlled via gas chromatography analyses of organic extracts from manufactured food pellets as previously described Moranis et al, 2012;Madore et al, 2014).…”

Section: Animalsmentioning

confidence: 99%

Amplification of mGlu₅-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

et al. 2017

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Energy-dense, yet nutritionally poor food is a high-risk factor for mental health disorders. This is of particular concern during adolescence, a period often associated with increased consumption of low nutritional content food and higher prevalence of mental health disorders. Indeed, there is an urgent need to understand the mechanisms linking unhealthy diet and mental disorders. Deficiency in n-3 polyunsaturated fatty acids (PUFAs) is a hallmark of poor nutrition and mood disorders. Here, we developed a mouse model of n-3 PUFA deficiency lasting from adolescence into adulthood. Starting nutritional deficits in dietary n-3 PUFAs during adolescence decreased n-3 PUFAs in both medial prefrontal cortex (mPFC) and nucleus accumbens, increased anxiety-like behavior, and decreased cognitive function in adulthood. Importantly, we discovered that endocannabinoid/mGlu 5 -mediated LTD in the mPFC and accumbens was abolished in adult n-3-deficient mice. Additionally, mPFC NMDAR-dependent LTP was also lacking in the n-3-deficient group. Pharmacological enhancement of the mGlu 5 /eCB signaling complex, by positive allosteric modulation of mGlu 5 or inhibition of endocannabinoid 2-arachidonylglycerol degradation, fully restored synaptic plasticity and normalized emotional and cognitive behaviors in malnourished adult mice. Our data support a model where nutrition is a key environmental factor influencing the working synaptic range into adulthood, long after the end of the perinatal period. These findings have important implications for the identification of nutritional risk factors for disease and design of new treatments for the behavioral deficits associated with nutritional n-3 PUFA deficiency.

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Section: Animalsmentioning

confidence: 99%

Amplification of mGlu₅-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

et al. 2017

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“…Low dietary intake of n-3 PUFA decreases DHA levels in the animal brain. As a result, emotional behavior (depressivelike symptoms and anxiety) as well as learning and memory are impaired as shown by us and others (Fedorova and Salem, 2006;Lafourcade et al, 2011;Moranis et al, 2011). On the opposite, positive effects of diet enriched in DHA on learning and memory have been demonstrated in laboratory animals (Gamoh et al, 1999;Yehuda et al, 1999;Carrie et al, 2002).…”

Section: Consequences Of the Decrease In N-3 Pufas On Age-related Neumentioning

confidence: 89%

“…In addition, mice exposed throughout life to a diet devoid of n-3 PUFAs displayed lower brain DHA level and higher LPSinduced IL-6 in the plasma and in the hippocampus (Mingam et al, 2008). With aging, IL-6 expression was increased in the cortex of both n-3 deficient and n-3 adequate mice while IL-10 expression was decreased with no effect of long term a-LNA deficient or enriched diet (Moranis et al, 2011) (figure 4). On the opposite, short term exposure to dietary EPA reduced IL-1-induced spatial memory deficit and anxiolytic behavior (Song et al, 2004;Song et al, 2008) and improved LPS and Ab-induced inhibition of long term potentiation (LTP) in both adult and aged rats .…”

Section: Consequences Of the Decrease In N-3 Pufas On Age-related Neumentioning

confidence: 96%

“…This state is called inflammaging at the periphery and in the brain. Recent clinical and experimental data obtained in our group have shown a strong association between blood proinflammatory cytokines levels, especially IL-6, quality of life and neuropsychiatric symptoms in a cohort of elderly subjects (Capuron et al, 2009;Capuron et al, 2011) and in aged laboratory mice (Moranis et al, 2011). The mechanisms underlying the effect of proinflammatory cytokine on mood and cognitive disorders have been intensively studied in rodents (Yirmiya and Goshen, 2011).…”

Section: Brain Innate Immune System In the Aging Brainmentioning

confidence: 99%

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Neuroinflammation and aging: influence of dietary n-3 polyunsaturated fatty acid

Layé

Delpech

Smedt-Peyrusse

et al. 2011

OCL

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“…In vivo, chronic dietary n-3 PUFA deficiency significantly increased the production and release of IL-6 and TNFα in the blood (McNamara et al, 2010) while it was not the case in adult and aged mice brain (Delpech et al, 2015a;Mingam et al, 2008;Moranis et al, 2012). However, DHA decrease in the brain during post-natal period strongly affects microglia activity (Madore et al, 2014).…”

Section: How Do N-3 Pufa Mechanisms Control Neuroinflammation?mentioning

confidence: 99%

N-3 PUFAs and neuroinflammatory processes in cognitive disorders

Leyrolle

Layé

Nadjar

2016

OCL

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-With the ageing population and increased cases of neurodegenerative diseases, there is a crucial need for the development of new nutritional approaches to prevent and delay the onset of cognitive decline. Neuroinflammatory processes contribute to neuronal damage that underpins neurodegenerative disorders. Growing evidence sheds light on the use of dietary n-3 long chain polyunsaturated fatty acids to improve cognitive performances and reduce the neuroinflammatory responses occurring with age and neurodegenerative pathologies. This review will summarise the most recent information related to the impact and mechanisms underlying the neuroinflammatory processes in cognitive disorders. We will also discuss the mechanisms underlying n-3 polyunsaturated fatty acids effect on neuroinflammation and memory decline.Keywords: Neuroinflammation / microglia / n-3 polyunsaturated fatty acids / cognitive disorders / Alzheimer disease Résumé -Acides gras polyinsaturés de la famille des oméga 3, processus neuroinflammatoires et troubles cognitifs. Le développement d'approches nutritionnelles pertinentes pour prévenir et retarder l'apparition du déclin cognitif est un enjeu important, compte tenu du vieillissement de la population et de l'augmentation de l'incidence des maladies neurodégénératives. Les processus neuro-inflammatoires contribuent aux mécanismes neuropathologiques impliqués dans les troubles neurodégénératifs et de la cognition. Des données récentes indiquent l'importance des acides gras polyinsaturés n-3 alimentaires dans le maintien des performances mnésiques et la régulation de la neuroinflammation liée à l'âge ou à la maladie d'Alzheimer. Dans cette revue, seront présentées des données récentes sur les liens existants entre le statut nutritionnel en acides gras polyinsaturés n-3, les processus neuro-inflammatoires et les troubles cognitifs associés, ainsi que les mécanismes qui pourraient être impliqués dans les effets protecteurs de ces acides gras.

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Long term adequate n-3 polyunsaturated fatty acid diet protects from depressive-like behavior but not from working memory disruption and brain cytokine expression in aged mice

Cited by 88 publications

References 93 publications

Amplification of mGlu₅-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

Amplification of mGlu₅-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

Neuroinflammation and aging: influence of dietary n-3 polyunsaturated fatty acid

N-3 PUFAs and neuroinflammatory processes in cognitive disorders

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Long term adequate n-3 polyunsaturated fatty acid diet protects from depressive-like behavior but not from working memory disruption and brain cytokine expression in aged mice

Cited by 88 publications

References 93 publications

Amplification of mGlu5-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

Amplification of mGlu5-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

Neuroinflammation and aging: influence of dietary n-3 polyunsaturated fatty acid

N-3 PUFAs and neuroinflammatory processes in cognitive disorders

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Product

Resources

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Amplification of mGlu₅-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance

Amplification of mGlu₅-Endocannabinoid Signaling Rescues Behavioral and Synaptic Deficits in a Mouse Model of Adolescent and Adult Dietary Polyunsaturated Fatty Acid Imbalance