Literatura científica selecionada sobre o tema "Récompenses naturelles"
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Artigos de revistas sobre o assunto "Récompenses naturelles"
Peacock, Shelley, Bharati Sethi, Allison Williams, Wendy Duggleby, Melanie Bayly, Jenny Swindle, Jenny Ploeg e Maureen Markle-Reid. "Older Adult Spouses with Multiple Chronic Conditions: Challenges, Rewards, and Coping Strategies". Canadian Journal on Aging / La Revue canadienne du vieillissement 36, n.º 2 (28 de março de 2017): 209–22. http://dx.doi.org/10.1017/s0714980817000095.
Texto completo da fonteLabbé St-Vincent, Simon, e André Blais. "Le vote à l’Élection d’à côté". Articles 35, n.º 1 (24 de março de 2016): 49–71. http://dx.doi.org/10.7202/1035792ar.
Texto completo da fonteTrébuchon, Jean-François. "Bois et Forêts des Tropiques, numéros spéciaux et nouveau comité éditorial". BOIS & FORETS DES TROPIQUES 356 (4 de setembro de 2023): 3. http://dx.doi.org/10.19182/bft2023.356.a37245.
Texto completo da fonteTeses / dissertações sobre o assunto "Récompenses naturelles"
Vicq, Eléonore. "Modulation nicotinique de l'activité dopaminergique et des comportements motivés". Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS135.
Texto completo da fonteSmoking affects one billion people worldwide, and is responsible for over 8 million preventable deaths a year, making it a major health concern. Nicotine, the main active compound in tobacco, acts on the nervous system by binding to nicotinic acetylcholine receptors (nAChRs). There is a wide diversity of nAChR subunits (��2 to 10 and β2 to 4) which assemble in different combinations to form pentameric receptors with different biophysical properties and localizations. Nicotine concomitantly produces rewarding and aversive effects, promoting and limiting nicotine consumption, respectively. While nAChRs are expressed in the reward system, notably the ventral tegmental area (VTA), they are also present in many other brain regions susceptible to nicotine-induced disruptions. The aim of my thesis work was to investigate the involvement of two non-canonical VTA-connected brain pathways in nicotine addiction: the pathways linking the interpeduncular nucleus (IPN) and the VTA, and the one connecting the VTA to the claustrum (CLA). I first studied the involvement of the IPN in nicotine reinforcement. We showed that IPN neurons respond heterogeneously to nicotine, and discovered that they are sensitive to low doses of nicotine that do not activate the VTA. Using new chemogenetic tools that I have developed, we have shown that β4-containing nAChRs of the IPN act as a brake on the response to nicotine in the VTA, thereby reducing the rewarding effects of the drug. The IPN would therefore contribute not only to aversion but also to nicotine reinforcement. Secondly, I studied how prolonged exposure to nicotine alters social interactions, and the potential involvement of the VTA-CLA pathway in these behavioral perturbations. We showed that chronic nicotine exposure increased the saliency of a novel social stimulus in a three-chamber task, resulting in an increased interaction time with novel conspecifics. Moreover, optogenetic activation of the VTA-CLA pathway induced a loss of preference for the novel social stimulus, while non-contingent optogenetic stimulation replicated the behavioral effects of prolonged nicotine exposure. Therefore, the VTA-CLA pathway seems to be involved in the saliency for new social stimuli, and this function may be disrupted by chronic nicotine exposure. Taken together, these studies highlight the importance of these two non-canonical pathways in nicotine addiction
Reisiger, Anne-Ruth. "Pathologie du système de récompense : effets à long terme d’une exposition chronique à la nicotine et au sucrose". Thesis, Bordeaux 1, 2013. http://www.theses.fr/2013BOR14870/document.
Texto completo da fonteLearning mechanisms associated with active responding for nicotine enhanced the excitability of the ILCx-BNST pathway. The objective of this project was to better understand the involvement of the ILCx-BNST pathway in nicotine self-administration. Since the endocannabinoid system controls nicotine reinforcement and nicotine-induced synaptic modifications, we examined the role of CB1 receptors in the BNST. We showed that acquisition of nicotine IVSA was associated with a persistent facilitation of LTP induction at ILCx-BNST synapses. Behaviorally, electrical stimulation temporarily increased excessive responding to nicotine when nicotine was not available. Moreover, using intra-BNST pharmacology, we revealed that stimulation of BNST CB1 receptors enhanced sensitivity to nicotine-paired cue. In contrast, after a prolonged history of nicotine intake, it blocked drug-seeking in a reinstatement model of relapse. Drug addiction is partly due to the inability to stop using despite negative consequences. The hypothesis that palatable food induces similar uncontrolled consumption is becoming more widespread. As drug addiction is known to increases activity of VTA DA neurons, we aimed to examine whether exposure to sucrose would induce similar neuronal modifications and impair the capacity to respond to an aversive stimulus. We found that sucrose enhanced spontaneous activity of DA VTA neurons. In addition, while a footshock caused a nearly complete inhibition of activity of VTA DA neurons in control rats, sucrose disrupted signaling of an aversive stimulus. These modifications were independent from the caloric state of the rats