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Université Victor Segalen Bordeaux 2, March 30th, 2010Organiser / Angelo Contarino

Abstract :


En France, une campagne de sensibilisation lancée en 2002 incite les gens à manger au moins 5 fruits et légumes par jour et à pratiquer l'équivalent d'une 1/2 heure de marche par jour (Programme national nutrition-santé). Des études ont mis en évidence le lien étroit entre l'alimentation,le bon fonctionnement du cerveau et l'équilibre émotionnel. Nos capacités cognitives, nos performances intellectuelles, notre mémorisation, ainsi que nos capacités d'apprentissage dépendent de nombreuses substances comme les sucres, les vitamines et minéraux, des acides aminés, des acides gras etc. De bonnes raisons pour la tenue de ce troisième Symposium "Alimentation et Neuroscience" organisé par Angelo Contarino. L'occasion pour ces 9 scientifiques de présenter leurs derniers travaux.
Symposium ouvert à tous (en anglais), pas d'inscription ! voir le progamme détaillé...


10h45-11h Welcome and presentation of sessions : Angelo Contarino

11h-11h30 Giovanni Marsicano
Affiliation: INSERM U862, NeuroCentre Magendie, Endocannabinoids and Neuroadaptation, Bordeaux, France.
Title: Bimodal Control of stimulated food intake by the endocannabinoid system

11h30-12h Guillaume Ferreira
Affiliation: Jeune Equipe "Nutrition, Inflammation et Cognition", Laboratoire Psynugen, UMR INRA 1286 - CNRS 5226 - Université Victor Segalen Bordeaux 2
Title: Behavioral and neurobiological mechanisms of conditioned food aversion and preference

12h-12h30 Angelo Contarino
Affiliation: Unité de Nutrition et Neurosciences, EA 2975, Université Bordeaux 1 et Victor Segalen Bordeaux 2
Title: Opiate withdrawal-related food intake: implication for the corticotropin-releasing factor system

12h30-13h Guy Simonnet and Jacques Philippe Moulinoux
Affiliation: Université Victor Ségalen Bordeaux 2 and UMR CNRS 5227, Bordeaux and EA 3891, Université Rennes 1, Rennes. France.
Title: Polyamine deficient diet: an innovative nutritional strategy for relieving pain

BUFFET

14h30-15h Martine Cador
Affiliation: CNRS UMR 5227, Team Neuropsychopharmacology of Addiction, Université Bordeaux 1 and Victor Segalen Bordeaux 2
Title: Sugar Overconsumption During Adolescence Selectively Alters Motivation and Reward Function in Adult Rats

15h-15h30 Benjamin Buaud
Affiliation: ITERG – Département Nutrition & Santé, Université Bordeaux 1, Talence, France
Title: A n-3 PUFA deficient diet generates alterations in vitamin A nuclear receptor expression: consequences on cognitive processes

15h30-16h Daniela Cota

Affiliation: INSERM U862, Avenir Group “Physiopathology of Energy Balance and Obesity”, Université de Bordeaux 2, Bordeaux, France.
Title: S6K1-dependent modulation of the hypothalamic melanocortin system.

16h-16h30 Fermin Milagro
Affiliation: Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona (Spain)
Title: Nutritional epigenetics

Speaker: Benjamin Buaud

Affiliation: ITERG – Département Nutrition & Santé, Université Bordeaux 1, Talence, France

Title: A n-3 PUFA deficient diet generates alterations in vitamin A nuclear receptor expression: consequences on cognitive processes

Abstract:
Background: N-3 polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid (DHA), are major components of the brain. Rats fed an n-3 PUFA deficient diet exhibit altered memory and learning capacities. Vitamin A via its nuclear receptors (RAR and RXR) plays a central role in the maintenance of such processes. Among its target genes, vitamin A controls the expression of neurogranin RC3 and neuromodulin GAP-43, two proteins considered as good markers of the dendrite spine density. Vitamin A and n-3 PUFA signaling pathways can interact (at least in part) via RXR and PPAR.
Objective: The present work deals with the hypothesis that an n-3 PUFA deficient diet could modify the expression of RC3 and GAP-43 by altering the expression pattern of RAR and RXR.
Procedures: Male Wistar rats at weaning were divided into two groups: the first one received a control diet (18:2n-6/18:3n-3=5.5), and the second one an n-3 PUFA deficient diet (18:2n-6/18:3n-3=232). After 3, 9, 18 and 25 weeks, RARb, RXRbg and PPARd mRNAs were quantified by real-time PCR in the striatum. The expression of RC3 and GAP-43 was estimated at mRNA and protein (western-blot) levels. Blood and brain fatty acid compositions were also investigated.
Results: From 18 weeks, RARb, RXRbg and PPARd mRNAs were simultaneously decreased in n-3 PUFA deficient rats. The expression of RC3 and GAP-43 was also diminished. In plasma, red blood cell membranes and brain phosphatidylethanolamine of the same rats, the docosapentaenoic acid percentage was strongly increased concomitantly to a decrease of that of the DHA.
Conclusion: The present results show that an n-3 PUFA deficient diet may induce changes in the expression pattern of vitamin A nuclear receptors, and by this way, lead to neurobiological alterations similar to those described during normal brain aging. These findings suggest that such a diet could probably accelerate establishment of the memory decline.


Speaker: Fermin Milagro

Affiliation: Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona (Spain)

Title: Nutritional epigenetics

Abstract:
The etiology of obesity is multifactorial, involving complex interactions among the genetic make-up, neuroendocrine status, fetal programming and different unhealthy environmental factors such as sedentarism or inadequate dietary habits. Among the different mechanisms that could lead to interindividual differences in obesity, epigenetics, defined as the study of heritable changes in gene expression that occur in the absence of a change in DNA sequence itself, has emerged in the last years as a very important determinant. Indeed, experimental evidences concerning dietary factors influencing obesity development through epigenetic mechanisms have been described. Thus, identification of those individuals that could present changes in the DNA methylation profiles, histone modifications on specific genes or other epigenetically-related processes could help to predict their susceptibility to later develop obesity o predict weight loss. Indeed, research concerning epigenetic mechanisms affecting weight homeostasis may allow to prevent weight gain and follow-up progress after weight loss, as well as to research and develop newer therapeutic approaches.

Speaker: Giovanni Marsicano

Affiliation: INSERM U862, NeuroCentre Magendie, Endocannabinoids and Neuroadaptation, Bordeaux, France.

Title: Bimodal Control of stimulated food intake by the endocannabinoid system

Abstract:
Activation of CB1 receptors is universally recognised as a powerful endogenous orexigenic signal, but the detailed underlying neuronal mechanisms are not fully understood. CB1 is expressed in different neuronal population, including GABAergic and glutamatergic neurons that control food consumption. Here, we investigated the differential role of CB1 in different neuronal populations on the regulation of stimulated food intake. We used conditional mouse mutant lines lacking CB1 expression mainly in cortical glutamatergic neurons (Glu-CB1-KO) or mainly in GABAergic neurons (GABA-CB1-KO), in combination with pharmacological approaches. In fasting-refeeding experiments, Glu-CB1-KO mice ate less than their wild type littermates, whereas GABA-CB1-KO showed a hyperphagic phenotype. In the same protocol, we tested two doses of the CB1 agonist Δ9-tetrahydrocannabinol (THC): one exerting an orexigenic effect (1mg/Kg), and one inducing hypophagia without affecting locomotion (2.5 mg/kg). The low hyperphagic dose of THC did not bear any effect in Glu-CB1-KO mice, whereas the hypophagic effect of the higher dose was blunted in GABA-CB1-KO mice. The same doses were fully reverted by allosteric enhancers of NMDA and GABAA receptors in wild-type mice, respectively. Further, the hypophagic effect of the higher dose of THC was inhibited by local blockade of CB1 signalling in the ventral striatum. These results indicate that CB1 receptors modulating excitatory transmission mediate well-known orexigenic effects of cannabinoids. Conversely, ventral striatal CB1 receptors are endowed with a hypophagic effect through inhibition of GABAergic transmission.



Speaker: Guillaume Ferreira

Affiliation: Jeune Equipe "Nutrition, Inflammation et Cognition", Laboratoire Psynugen, UMR INRA 1286 - CNRS 5226 - Université Victor Segalen Bordeaux 2

Title: Behavioral and neurobiological mechanisms of conditioned food aversion and preference

Abstract:
Food choices are mainly based on learned flavor preferences and aversions. These correspond to associative learning from the chemosensory cues of food, i.e. odor and taste, to the beneficial or deleterious digestive consequences. When ingestion of new flavored food leads to an important energy intake, subsequently that flavor is liked and preferred. The contrary applies: if the consumption generates a visceral malaise, that flavor will be disliked and avoided. This talk will address the learning and memory processes involved in these changes of hedonic value, beginning from food aversion learning in rodents, which has been the most extensively studied phenomenon, to finish by appetitive learning. First, I will describe the peculiar behavioural characteristics of conditioned odor and taste aversions. I will also discuss the long-term impact of early flavor experiences on these aversive learning in adults. Then, I will address the neural substrates involved in food aversion memory, focusing on two forebrain structures, the insular cortex and the basolateral amygdala, where olfactory, gustatory and visceral information converge. I will present their respective roles in the different steps of aversive odor and taste memory formation. Finally I will deal with flavor preference memory (sucrose-conditioned odor preference), showing how appetitive flavor experiences modify odor-taste convergence onto single neurons in amygdala and insular cortex.

Speaker: Guy Simonnet and Jacques Philippe Moulinoux

Affiliation: Université Victor Ségalen Bordeaux 2 and UMR CNRS 5227, Bordeaux and EA 3891, Université Rennes 1, Rennes. France.

Title: Polyamine deficient diet: an innovative nutritional strategy for relieving pain

Abstract:
There is a compelling evidence body that N-methyl-D-aspartate receptors (NMDA-R) play a critical role in the development and maintenance of pain hypersensitivity leading to both exaggerated postoperative pain and chronic pain. However, long-term treatments with NMDA-R antagonists are limited in humans by unacceptable side-effects. To avoid these deleterious effects, an alternative strategy could be to negatively modulate NMDA-R functioning without blocking their physiological activity. Since polyamines positively modulate the functioning of NMDA-R and mainly originate from normal dietary intake and bacterial metabolism in the gut, we developed a nutritional therapy based on dietary polyamine deficiency. Pre-clinical and some preliminary clinical results will be shown and discussed.



Speaker: Daniela Cota

Affiliation: INSERM U862, Avenir Group “Physiopathology of Energy Balance and Obesity”, Université de Bordeaux 2, Bordeaux, France.

Title: S6K1-dependent modulation of the hypothalamic melanocortin system.

Abstract:
We have recently demonstrated that the Mammalian Target Of Rapamycin (mTOR) signaling pathway plays a role in the hypothalamic mechanisms that respond to nutrient availability, regulating energy balance (Cota D et al., Science, 2006). In particular, under free-fed conditions, the mTOR downstream target S6 kinase 1 (S6K1) is activated (phosphorylated) in both Pro-opio-melanocortin (POMC)- and Agouti-related protein (AgRP)- expressing neurons in the arcuate nucleus (ARC) of the hypothalamus. POMC and AgRP produced in the ARC oppositely regulate the activity of melanocortin receptors located in the hypothalamic paraventricular nucleus (PVN), all together forming the hypothalamic melanocortin system. We therefore used mice lacking S6K1 (S6K1-/-) to investigate the role of this kinase in the control of hypothalamic melanocortin activity.
Under free-fed conditions, S6K1-/- mice eat slightly, but significantly more than their wild-type (WT) littermates. This increase in food consumption becomes even more evident after fasting-induced re-feeding, a condition known to activate melanocortin POMC neurons. Interestingly, S6K1-/- mice have significantly less POMC-labeled cells in the ARC, which is associated to a reduction in POMC-labeled projections in the PVN. In addition, S6K1-/- mice show increased AgRP-labeled projections in the PVN. Differently from WT littermates, S6K1-/- mice do not respond neither to the anorectic action of MTII (a melanocortin agonist), nor to the orectic action of AgRP, when these compounds are administered intracerebroventricularly. Ongoing studies are currently evaluating the activity of the melanocortin system after fasting and re-feeding, using markers of early neuronal activation (c-fos) and electrophysiological recordings at the level of the PVN. The present findings so far suggest that S6K1 might control food intake by regulating the hypothalamic melanocortin system function.



Speaker: Angelo Contarino

Affiliation: Unité de Nutrition et Neurosciences, EA 2975, Université Bordeaux 1 et Victor Segalen Bordeaux 2

Title: Opiate withdrawal-related food intake: implication for the corticotropin-releasing factor system

Abstract:
The opiate withdrawal syndrome is characterised by somatic and negative affective-like signs and symptoms. Avoidance of and/or escape for the opiate withdrawal malaise strongly motivate continued drug intake and abuse. Activation of stress-responsive systems plays a key role in the expression of the myriad of somatic and affective-like features of the opiate withdrawal syndrome. The corticotropin-releasing factor system is a major component of stress-responsive systems, and mediates somatic and affective-like features of the opiate withdrawal syndrome. The opiate withdrawal syndrome has also been associated with decreased intake, preference or motivation for foods with varying degrees of palatability. Using genetically modified mice, in the present study we examined the implication for the corticotropin-releasing factor system and other stress-responsive systems in food intake alterations associated with opiate withdrawal.

Speaker: Martine Cador

Affiliation: CNRS UMR 5227, Team Neuropsychopharmacology of Addiction, Université Bordeaux 1 and Victor Segalen Bordeaux 2

Title: Sugar Overconsumption During Adolescence Selectively Alters Motivation and Reward Function in Adult Rats

Abstract:

There has been a dramatic escalation in sugar intake in the last few decades, most strikingly observed in the adolescent population. Sugar overconsumption has been associated with several adverse health consequences, including obesity and diabetes. Very little is known, however, about the impact of sugar overconsumption on mental health, in general, and on reward-related behavioral disorders, in particular. We examined in rats the effects of unlimited access to sucrose during adolescence on the motivation for natural and pharmacological rewards in adulthood. We found that sugar overconsumption during adolescence, but not during adulthood, reduced the subsequent motivation for saccharin and maltodextrin, but not cocaine. This selective decrease in motivation is more likely due to changes in brain reward processing rather than changes in gustatory perception. Sugar overconsumption induces a developmental stage specific chronic depression in reward processing that may contribute to an increase in the vulnerability to reward-related psychiatric disorders.