L'absence du transporteur intestinal de di/tripeptides PepT1 induit le développement d'un état pré-diabétique et anxio-dépressif

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L'absence du transporteur intestinal de di/tripeptides PepT1 induit le développement d'un état pré-diabétique et anxio-dépressif

International audienc

Paternal transmission of vulnerability to high fat diet-induced metabolic and neurobehavioural impairments

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Effect of Food Restriction on Energy Expenditure of Monosodium Glutamate-Induced Obese Rats

The neonatal administration of monosodium glutamate (MSG) to rodents leads to obesity in the adult animal, characterized by increased fat storages. Chronic food restriction is known to induce reduction in body energy expenditure, as an adaptive mechanism to save energy. Our purpose was to examine whether obesity can alter the mechanism of energy conservation in food-restricted animals. Newborn female Wistar rats were injected either MSG (obese) or saline (control). At the age of 90 days, the animals were fed daily ad libitum (control and MSG) or restricted (50%) (control-restricted and MSG-restricted). After 30 days the animals were sacrificed and the energy balance was determined by calorimetric analysis. Some parameters of energy balance and body composition were affected by MSG treatment as well as food restriction. the percent reduction of the energy expenditure and fat content in MSG-restricted animals was lower than control-restricted animals, when compared with their respective ad libitum groups. These results indicate that all food-restricted animals were able to develop the mechanism of energy conservation, regardless of the obesity, but it was less efficient in MSG-obese animals. Copyright (C) 2009 S. Karger AG, BaselConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Physiol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, BR-04023900 São Paulo, BrazilWeb of Scienc

Co-activation of VTA DA and GABA neurons mediates nicotine reinforcement

International audienceSmoking is the most important preventable cause of mortality and morbidity worldwide. This nicotine addiction is mediated through the nicotinic acetylcholine receptor (nAChR), expressed on most neurons, and also many other organs in the body. Even within the ventral tegmental area (VTA), the key brain area responsible for the reinforcing properties of all drugs of abuse, nicotine acts on several different cell types and afferents. Identifying the precise action of nicotine on this microcircuit, in vivo, is important to understand reinforcement, and finally to develop efficient smoking cessation treatments. We used a novel lentiviral system to re-express exclusively high-affinity nAChRs on either dopaminergic (DAergic) or gamma-aminobutyric acid-releasing (GABAergic) neurons, or both, in the VTA. Using in vivo electrophysiology, we show that, contrary to widely accepted models, the activation of GABA neurons in the VTA plays a crucial role in the control of nicotine-elicited DAergic activity. Our results demonstrate that both positive and negative motivational values are transmitted through the dopamine (DA) neuron, but that the concerted activity of DA and GABA systems is necessary for the reinforcing actions of nicotine through burst firing of DA neurons. This work identifies the GABAergic interneuron as a potential target for smoking cessation drug development