Du calcul réfléchi à la multiplication posée

L’observation de difficultés d’élèves de cycle 3 dans la réalisation de l’algorithme de la multiplication posée amène à se demander quel continuum existe entre calcul réfléchi et techniques opératoires. Dans quelle mesure les élèves de cycle 3 font-ils appel au calcul réfléchi dans la réalisation de la multiplication posée? Les programmes préconisent l’établissement d’un lien étroit entre apprentissage des techniques opératoires, propriétés et sens des opérations. Ce travail sur le sens et les propriétés passe par la pratique du calcul réfléchi. Instaurer des allers-retours entre technique automatisée et pratique réfléchie semble indispensable, or l’apprentissage de la multiplication posée emprunte une direction : du calcul réfléchi vers l’opération posée. Notre protocole propose d’emprunter la direction inverse : partir d’une réalisation automatique, pour parvenir à une approche plus réfléchie en imposant de la nécessité de reconnaître les calculs intermédiaires. L’expérimentation a permis de montrer comment des élèves de cycle 3 pouvaient passer d'une méthode automatique apprise en classe, dont le sens a été perdu de vue, à un travail faisant appel à une réflexion retrouvée sur le sens

Cognitive Dysfunction, Affective States, and Vulnerability to Nicotine Addiction: A Multifactorial Perspective

International audienceAlthough smoking prevalence has declined in recent years, certain subpopulations continue to smoke at disproportionately high rates and show resistance to cessation treatments. Individuals showing cognitive and affective impairments, including emotional distress and deficits in attention, memory, and inhibitory control, particularly in the context of psychiatric conditions, such as attention-deficit hyperactivity disorder, schizophrenia, and mood disorders, are at higher risk for tobacco addiction. Nicotine has been shown to improve cognitive and emotional processing in some conditions, including during tobacco abstinence. Self-medication of cognitive deficits or negative affect has been proposed to underlie high rates of tobacco smoking among people with psychiatric disorders. However, pre-existing cognitive and mood disorders may also influence the development and maintenance of nicotine dependence, by biasing nicotine-induced alterations in information processing and associative learning, decision-making, and inhibitory control. Here, we discuss the potential forms of contribution of cognitive and affective deficits to nicotine addiction-related processes, by reviewing major clinical and preclinical studies investigating either the procognitive and therapeutic action of nicotine or the putative primary role of cognitive and emotional impairments in addiction-like features

Rôle des récepteurs nicotiniques neuronaux de l'acétylcholine dans la dépendance à la nicotine

La nicotine agit via les récepteurs nicotiniques de l acétylcholine (nAchRs). L invalidation des nAChRs contenant la sous-unité b2 (nAChRs*b2) bloque l autoadministration de nicotine, restaurée par la réexpression de b2 au sein de l aire tegmentale ventrale (ATV) chez les souris nulles pour cette sous-unité (b2-/-). A l inverse, les souris nulles pour la sous-unité a7 s autoadministrent la nicotine et répondent à celle-ci par une augmentation de la libération de dopamine dans le noyau accumbens. Cependant, le sevrage induit par la cessation de l administration chronique de nicotine est normal chez les souris b2-/-. A long terme, l exposition à la nicotine ne modifie pas l activité dopaminergique dans l ATV ou l activité exploratoire, grâce à un processus qui implique les nAChRs*a7. En outre, chez les souris b2-/-, la nicotine entraîne, via les nAChRs*a7, une restauration de ces fonctions. Cette étude offre une meilleure compréhension des processus de la dépendance à la nicotine.PARIS-BIUSJ-Thèses (751052125) / SudocPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus

International audienceKeywords: In vivo amyloid pathology Amyloid precursor protein a7 nicotinic receptor b2 nicotinic receptor Memory deficit Hippocampus a b s t r a c t Alzheimer's disease (AD) is characterized by the presence of plaques and tangles. Only certain brain regions are vulnerable to progressive neurodegeneration. It is therefore important to study the contribution of key brain structures to AD pathology. Here, we investigated the consequences of amyloid accumulation specifically in dentate gyrus (DG). This was obtained with viral transduction of human amyloid precursor protein harboring 3 pathogenic mutations (hAPP-SLA, Swedish, London, and Austrian) in DG. Adult wild-type C57Bl/6J mice exhibited long-term expression of hAPP-SLA, synthesis and deposition of oligomeric amyloid beta (Ab), and associated memory impairment. We then investigated the role of a7 or b2 subunits of the nicotinic acetylcholine receptor by transducing hAPP-SLA into C57Bl/ 6J mice knockout (KO) for a7 or b2 subunits. b2 KO mice did not exhibit memory loss induced by hAPP-SLA expression, whereas aged mice lacking the a7 subunit displayed a hAPP-SLA independent cognitive deficit. The present data reveal a role for b2 containing nicotinic acetylcholine receptors in the memory deficits associated with DG specific amyloid beta expression

Variability and vulnerability to comorbid conditions in addictive disorders

Addictive disorders are a major burden worldwide, including high mortality rates. Part of this burden can be attributed to comorbid psychiatric disorders, especially suicidal behavior. Our project aims at characterizing the genetic and clinical vulnerability associated with the comorbidity between addictive and psychiatric disorders, focusing on suicidal risk

A low dose of nicotine is sufficient to produce nicotine withdrawal in mice.

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Profound alteration in reward processing due to a human polymorphism in CHRNA5: a role in alcohol dependence and feeding behavior

International audienceHuman genetic variation in the nicotinic receptor gene cluster CHRNA5/A3/B4, in particular the non-synonymous and frequent CHRNA5 variant rs16969968 (α5SNP), has an important consequence on smoking behavior in humans. A number of genetic association studies have additionally implicated the CHRNA5 gene in addictions to other drugs, and also body mass index (BMI). Here, we model the α5SNP, in a transgenic rat line, and establish its role in alcohol dependence, and feeding behavior. Rats expressing the α5SNP consume more alcohol, and exhibit increased relapse to alcohol seeking after abstinence. This high-relapsing phenotype is reflected in altered activity in the insula, linked to interoception, as established using c-Fos immunostaining. Similarly, relapse to food seeking is increased in the transgenic group, while a nicotine treatment reduces relapse in both transgenic and control rats. These findings point to a general role of this human polymorphism in reward processing, and multiple addictions other than smoking. This could pave the way for the use of medication targeting the nicotinic receptor in the treatment of alcohol use and eating disorders, and comorbid conditions in smokers

Spatial learning in Long-Evans Hooded rats and C57BL/6J mice: different strategies for different performance.

International audienceSpatial learning abilities of rodents have been extensively used to explore the management of a wide range of cognitive and emotional processes such as learning, memory, attention and anxiety. Knowledge about the organization and processing of spatial learning has mainly been obtained in rats. Due to increasing generation of genetically modified mice, cognitive abilities of mice are now extensively tested. The present paper aimed at comparing spatial representation, learning and strategies in C57BL/6J mice and Long-Evans Hooded rats when subjected to the same spatial learning paradigm, i.e. learning a food location in a crossmaze. We also analyzed the influence of environmental richness on learning modalities in both species. Our results showed that rats and mice could exhibit similar spatial learning abilities in some circumstances. However, Long-Evans rats and C57BL/6J mice may set up different strategies depending on the availability of visual information within the environment. Rats' learning strategies mainly relied on distant visual cues and seemed more efficient than those used by mice as they needed less time than mice to solve the task. We emphasize that the strategies of mice are less robust and flexible than the ones set up by rats. Finally, the richness of the environment was shown to affect speed and quality of spatial learning in both species

Reinforcing effects of nicotine microinjections into the ventral tegmental area of mice: dependence on cholinergic nicotinic and dopaminergic D1 receptors.

International audienceWe used an intracranial self-administration (ICSA) procedure to assess the involvement of the ventral tegmental area (VTA) nicotinic receptors in the rewarding effects of nicotine. We then challenged intra-VTA nicotine self-administration via systemic or local injections of dopamine (DA)-D1 and nicotinic receptor antagonists. C57BL/6J mice were stereotaxically implanted unilaterally with a guide cannula above the VTA. After 1 week of recovery, mice were allowed to discriminate between two arms of a Y-maze over seven daily sessions, one arm being reinforced by intracranial nicotine microinjection. Mice exhibited nicotine self-administration at both doses tested, i.e. 10 ng (21.6 pmol) and 100 ng (216 pmol)/50-nl injection. In contrast, mice receiving a 216-pmol nicotine dose 0.8 mm above VTA performed at chance level. Once the ICSA response was acquired, systemic pretreatment with the DA-D1 receptor antagonist SCH 23390 (25 microg/kg i.p.) or co-infusion of the nAChR antagonist DHbetaE with nicotine disrupted ICSA. Replacement of SCH 23390 by vehicle, or withdrawal of DHbetaE from nicotine/DHbetaE mixed solutions led to recovery of intra-VTA nicotine self-administration. We conclude that nicotinic receptors in the VTA, presumably alpha4beta2 nAChRs are critically to mediate the rewarding effects of nicotine and that DA-D1 receptors are also directly implicated