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  • Sophie Layé et al. dans JNeurosci

    18 juin 2017

    la nutrition est un facteur environnemental clé

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    4 sept. 2017

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  • G. Ferreira, P. Trifilieff et al. dans eNeuro

    22 juin 2017

    changements significatifs sur le long terme...

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    29 juin 2017

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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 acids imbalance.Amplification of mGlu5-endocannabinoid signaling rescues behavioral and synaptic deficits in a mouse model of adolescent and adult dietary polyunsaturated fatty acids imbalance.
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 acid (PUFAs) is a hallmark of poor nutrition and mood disorders. Here, we developed a mouse model of n-3 PUFAs 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/mGlu5-mediated long-term depression in the mPFC and accumbens was abolished in adult n-3-deficient mice. Additionally, mPFC NMDAR-dependent long-term potentiation was also lacking in the n-3-deficient group. Pharmacological enhancement of the mGlu5/eCB signaling complex, by positive allosteric modulation of mGlu5 or inhibition of endocannabinoid 2-arachidonylglycerol (2-AG) 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 PUFAs' deficiency.SIGNIFICANCE STATEMENTIn a mouse model mimicking n-3 PUFAs dietary deficiency during adolescence and adulthood, we found strong increases in anxiety and anhedonia which lead to decreases in specific cognitive functions in adulthood. We found that endocannabinoid/mGlu5-mediated long-term depression and NMDAR-dependent long-term potentiation were lacking in adult n-3 deficient mice. Acute positive allosteric modulation of mGlu5 or inhibition of endocannabinoid degradation normalized behaviors and synaptic functions in n-3 PUFA-deficient adult mice. These findings have important implications for the identification of nutritional risk for disease and the design of new treatments for the behavioral deficits associated with nutritional n-3 PUFAs' imbalance.
Manduca A, Bara A, Larrieu T, Lassalle O, Joffre C, Layé S, Manzoni OJ.
J Neurosci. 2017 Jun 19

How Hyperarousal and Sleep Reactivity Are Represented in Different Adult Age Groups: Results from a Large Cohort Study on Insomnia.How Hyperarousal and Sleep Reactivity Are Represented in Different Adult Age Groups: Results from a Large Cohort Study on Insomnia.
Hyperarousal is a 24-h state of elevated cognitive and physiological activation, and is a core feature of insomnia. The extent to which sleep quality is affected by stressful events-so-called sleep reactivity-is a vulnerability factor for developing insomnia. Given the increasing prevalence of insomnia with age, we aimed to investigate how hyperarousal and sleep reactivity were related to insomnia severity in different adult age groups. Data were derived from a large cohort study investigating the natural history of insomnia in a population-based sample (n = 1693). Baseline data of the Arousal Predisposition Scale (APS) and Ford Insomnia Response to Stress Test (FIRST) were examined across age and sleep/insomnia subgroups: 25-35 (n = 448), 35-45 (n = 528), and 45-55 year olds (n = 717); good sleepers (n = 931), individuals with insomnia symptoms (n = 450), and individuals with an insomnia syndrome (n = 312). Results from factorial analyses of variance (ANOVA) showed that APS scores decreased with increasing age, but increased with more severe sleep problems. FIRST scores were not significantly different across age groups, but showed the same strong increase as a function of sleep problem severity. The findings indicate that though arousal predisposition and sleep reactivity increase with more severe sleep problems, only arousal decreases with age. How arousing events affect an individual during daytime thus decreases with age, but how this arousal disrupts sleep is equivalent across different adult age groups. The main implication of these findings is that treatment of insomnia could be adapted for different age groups and take into consideration vulnerability factors such as hyperarousal and stress reactivity.
Altena E, Chen IY, Daviaux Y, Ivers H, Philip P, Morin CM.
Brain Sci. 2017 Apr 14

Inducing a long-term potentiation in the dentate gyrus is sufficient to produce rapid antidepressant-like effects.Inducing a long-term potentiation in the dentate gyrus is sufficient to produce rapid antidepressant-like effects.
Recent hypotheses propose that one prerequisite to obtain a rapid antidepressant (AD) effect would reside in processes of synaptic reinforcement occurring within the dentate gyrus (DG) of the hippocampus independently from neurogenesis. However, to date no relationship has been established between an increased DG synaptic plasticity, and rapid AD-like action. To the best of our knowledge, this study shows for the first time that inducing a long-term potentiation (LTP) within the DG by stimulating the perforant pathway (PP) is sufficient to induce such effects. Thus, Sprague-Dawley rats having undergone a successful LTP displayed a significant reduction of immobility when passed acutely 3 days thereafter in the forced swimming test (FST). Further, in a longitudinal paradigm using the pseudo-depressed Wistar-Kyoto rat strain, LTP elicited a decrease of FST immobility after only 2 days, whereas the AD desipramine was not effective before 16 days. In both models, the influence of LTP was transient, as it was no more observed after 8-9 days. No effects were observed on the locomotor activity or on anxiety-related behavior. Theta-burst stimulation of a brain region anatomically adjacent to the PP remained ineffective in the FST. Immunoreactivity of DG cells for phosphorylated histone H3 and doublecortin were not modified three days after LTP, indicating a lack of effect on both cell proliferation and neurogenesis. Finally, depleting brain serotonin contents reduced the success rate of LTP but did not affect its subsequent AD-like effects. These results confirm the 'plastic DG' theory of rapid AD efficacy. Beyond, they point out stimulations of the entorhinal cortex, from which the PP originates, as putative new approaches in AD research.
Kanzari A, Bourcier-Lucas C, Freyssin A, Abrous DN, Haddjeri N, Lucas G.
Mol Psychiatry. 2017 May 9

MicroRNA and chronic pain: From mechanisms to therapeutic potential.MicroRNA and chronic pain: From mechanisms to therapeutic potential.
Chronic pain is a major public health issue with an incidence of 20-25% worldwide that can take different forms like neuropathic, cancer-related or inflammatory pain. Chronic pain often limits patients in their daily activities leading to despair. Thus, the goal of treatments is to relieve pain sufficiently to enable patients to go back to a normal life. Unfortunately, few patients with chronic pain obtain complete relief from the analgesics that are currently available. It is thus of prime importance to get a better understanding of chronic pain mechanisms to design new therapeutic strategies and pain-killers. In this sense, the study of microRNA (miRNAs) in chronic pain conditions could lead to a breakthrough in pain management. miRNAs have emerged as master regulators of gene expression in the nervous system where they contribute to neuronal network plasticity. The involvement of miRNAs in the maladaptive plasticity mechanisms of chronic pain is now well documented. Here, we review studies conducted in different animal models and in patients that screened chronic pain-related miRNAs and their targets. Clinical studies suggest that miRNAs expression could reflect the high variability among pain patients that could help to categorize patients and finally lead to personalized therapies. We also point out the different strategies investigated to design miRNA-based analgesics. Finally, we highlight the current miRNA-based clinical trials to hypothesize their potential as therapeutic tool for chronic pain.
López-González MJ, Landry M, Favereaux A.
Pharmacol Ther. 2017 Jun 1

Operation and plasticity of hippocampal CA3 circuits: implications for memory encodingOperation and plasticity of hippocampal CA3 circuits: implications for memory encoding
The CA3 region of the hippocampus is important for rapid encoding of memory. Computational theories have proposed specific roles in hippocampal function and memory for the sparse inputs from the dentate gyrus to CA3 and for the extended local recurrent connectivity that gives rise to the CA3 autoassociative network. Recently, we have gained considerable new insight into the operation and plasticity of CA3 circuits, including the identification of novel forms of synaptic plasticity and their underlying mechanisms, and structural plasticity in the GABAergic control of CA3 circuits. In addition, experimental links between synaptic plasticity of CA3 circuits and memory are starting to emerge.
Rebola N, Carta M, Mulle C.
Nat Rev Neurosci. 2017 Apr. Review

Optimized labeling of membrane proteins for applications to super-resolution imaging in confined cellular environments using monomeric streptavidin.Optimized labeling of membrane proteins for applications to super-resolution imaging in confined cellular environments using monomeric streptavidin.
Recent progress in super-resolution imaging (SRI) has created a strong need to improve protein labeling with probes of small size that minimize the target-to-label distance, increase labeling density, and efficiently penetrate thick biological tissues. This protocol describes a method for labeling genetically modified proteins incorporating a small biotin acceptor peptide with a 3-nm fluorescent probe, monomeric streptavidin. We show how to express, purify, and conjugate the probe to organic dyes with different fluorescent properties, and how to label selectively biotinylated membrane proteins for SRI techniques (point accumulation in nanoscale topography (PAINT), stimulated emission depletion (STED), stochastic optical reconstruction microscopy (STORM)). This method is complementary to the previously described anti-GFP-nanobody/SNAP-tag strategies, with the main advantage being that it requires only a short 15-amino-acid tag, and can thus be used with proteins resistant to fusion with large tags and for multicolor imaging. The protocol requires standard molecular biology/biochemistry equipment, making it easily accessible for laboratories with only basic skills in cell biology and biochemistry. The production/purification/conjugation steps take ∼5 d, and labeling takes a few minutes to an hour.
Chamma I, Rossier O, Giannone G, Thoumine O, Sainlos M.
Nat Protoc. 2017 Apr

Brèves...

Un plan sévère d’économies

18 juil. 2017

... les universités savent qu’elles n’échapperont pas à la cure annoncée par Bercy. Reste que l’ampleur des annulations va bien au-delà de ce qui étai...► Lire la suite

L'IRM Iseult: la plus grande machine de ce type dans le monde

11 juil. 2017

Il produira un champ magnétique de 11,7 teslas, soit quatre fois plus que les scanners de diagnostic actuellement en service dans les hôpitaux françai...► Lire la suite

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