4 research outputs found

    Gli effetti della caffeina sul divertimento, sulla velocitĂ  di lettura e sull'ampliamento della rete semantica: Uno studio crossover randomizzato in doppio cieco

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    La caffeina quale sostanza psicostimolante ha spesso incitato l’interesse della comunità scientifica per i potenziali benefici che potrebbe comportare in termini di miglioramenti della prestazione psicofisica. Obiettivi: lo scopo di questo studio sperimentale è stato quello di indagare gli effetti positivi della caffeina su specifiche abilità cognitive. In particolare, questo elaborato riporta i risultati su come la caffeina influisce sulle emozioni percepite, sul divertimento, sulla velocità di lettura e sull’ampliamento della rete semantica. Metodi: lo studio meccanicistico è stato realizzato in doppio cieco. Lo studio prevedeva il coinvolgimento dei partecipanti in due momenti. In entrambi i momenti ai partecipanti era chiesto di assumere una bevanda; solo in uno dei due incontri era disciolta nella bevanda una dose da 200 mg di caffeina. I due incontri sono stati programmati a distanza di una settimana l’uno dall’altro e alla stessa ora, nel corso della mattinata. Risultati: una singola dose di caffeina non influisce sull’eccitazione e sullo stato di ansia, ma risulta essere significativo il momento di somministrazione, prima e alla fine della somministrazione. La caffeina non sembra aver influenzato l’eccitazione del partecipante, ma sembra averne influenzato l’emozione, per cui si è rilevato un dato interessante sul divertimento post gioco. Questo miglioramento è stato accompagnato da una maggior velocità di lettura del testo. Inoltre, la caffeina facilita l’esecuzione di compiti dove si debbano connettere fra loro in modo rapido e accurato informazioni semantiche. Conclusioni: questi risultati mostrano che una piccola quantità di caffeina potrebbe migliorare diverse funzioni cognitive, stimolando un circuito che sottostà e coinvolge queste funzioni cognitive, ovvero emozioni, lettura e semantica.Caffeine as a psychostimulating substance has often aroused the interest of the scientific community for the potential benefits it could bring in terms of improvements in psychophysical performance. Objectives: The purpose of this experimental study was to investigate the positive effects of caffeine on specific cognitive abilities. Specifically, this paper reports results on how caffeine affects perceived emotions, enjoyment, reading speed, and semantic network expansion. Methods: the mechanistic study was double-blinded. The study involved engaging participants at two time points. At both times, participants were asked to take a drink; only in one of the two encounters was a 200mg dose of caffeine dissolved in the drink. The two encounters were scheduled one week apart and at the same time in the morning. Results: a single dose of caffeine did not affect arousal and anxiety state, but the timing of administration, before and at the end of administration, appears to be significant. Caffeine does not seem to have affected the participant's arousal, but it does seem to have affected the participant's excitement, so there was an interesting finding on postgame enjoyment. This improvement was accompanied by increased speed of reading text. In addition, caffeine facilitates the performance of tasks where semantic information has to be connected together quickly and accurately. Conclusions: these results show that a small amount of caffeine could improve several cognitive functions by stimulating a circuit underlying and involving these cognitive functions, namely emotion, reading and semantics

    Identifying Mechanisms Underlying the Association between Attention- Deficit/Hyperactivity Disorder and Problematic Alcohol Use in College Students

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    Students with ADHD represent a significant population on college campuses who have been found to be at risk for problematic alcohol use. Yet little is known about mechanisms underlying the association between ADHD and alcohol-related problems. We examined patterns and consequences of alcohol use in college students with and without ADHD, as well as three possible mediators of the association between ADHD and alcohol-related impairment: (1) self-reported difficulty stopping a drinking session, (2) cue dependency on a behavioral task of response inhibition, and (3) self-reported trait disinhibition. Participants with ADHD reported higher rates of negative consequences of alcohol use relative to the non-ADHD group, despite equivalent rates of alcohol use. In addition, the ADHD group had higher rates of difficulty stopping a drinking session. Difficulty stopping a drinking session mediated the relationship between ADHD and negative consequences of alcohol use. Cue dependency and trait disinhibition did not mediate this relationship. These findings indicate that college students with ADHD are experiencing higher rates of negative consequences of alcohol use relative to their peers without ADHD. Difficulty stopping a drinking session may be one mechanism that explains the relationship between ADHD and alcohol-related problems

    Développement d'un modèle animal chez le rat reproduisant un déficit motivationnel pouvant s'apparenter à un syndrome d'apathie de la maladie de Parkinson

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    A côté de la triade motrice symptomatologique de la maladie de Parkinson (MP), des troubles comportementaux et cognitifs sont également fréquemment observés, incluant notamment l'apathie, définie comme une importante diminution des comportements motivés et qui est souvent associée à de l'anxiété et de la dépression. De façon intéressante, ces troubles neuropsychiatriques sont souvent observés chez des patients parkinsoniens traités par la stimulation cérébrale à haute fréquence du noyau sous-thalamique. Bien que les mécanismes physiopathologiques à l'origine de ces troubles restent aujourd'hui encore inconnus, il a été récemment suggéré qu'il pouvait exister un lien entre la diminution du traitement dopaminergique (DA) (rendue possible par les effets bénéfiques sur le plan moteur de la stimulation cérébrale profonde) et la résurgence du syndrome d'apathie chez ces patients parkinsoniens stimulés. Dans une première partie expérimentale, nous avons voulu déterminer le rôle du système DA dans l'émergence de ces troubles neuropsychiatriques d'identifier les projections DA ascendantes qui pourraient préférentiellement être impliquées. Notre modèle animal chez le rat, obtenu par des lésions neurotoxiques sélectives, bilatérales et partielles des différentes régions du continuum DA mésencéphalique nous a permis de mettre en évidence un rôle déterminant de la voie DA nigrostriatale dans les processus motivationnels et dans la régulation des comportements de type dépressif et anxieux, tout en s'affranchissant d'une altération des fonctions motrices. Dans une deuxième partie, une approche pharmacologique par des traitements chroniques à la L-DOPA ou au Ropinirole (agoniste D2/D3) nous a permis de vérifier de la bonne valeur prédictive de notre modèle animal vis-à-vis des traitements utilisés en clinique. L'administration de différents agonistes DA sélectifs des récepteurs de type D1, D2 et D3 nous a permis par la suite de montrer une implication majeure des récepteurs D3 dans la capacité à corriger le phénotype induit par la lésion de la voie nigrostriatale, ce qui ouvre ainsi la voie à de nouvelle cible thérapeutique. Au final, les données obtenues au cours de ce travail doctoral apportent de nouveaux arguments en faveur d'une implication de la voie DA nigrostriée dans l'émergence des troubles apathiques. Le modèle lésionnel mis en place pourra permettre de mieux appréhender le rôle de la dopamine dans les processus qui sous-tendent ces troubles motivationnels et thymiques dans la MP et identifier de nouvelles stratégies thérapeutiques mieux adaptées pour leur traitement.Beyond the classical triad of motor symptoms observed in Parkinson's disease (PD), behavioural and cognitive disturbances are also commonly observed, including apathy, defined as a decrease in motivated directed behaviours, and which is often associated with anxiety and depression. Interestingly, these neuropsychiatric symptoms are frequently observed in parkinsonian patients with high frequency stimulation of the subthalamic nucleus. Although the pathophysiological mechanisms behind these troubles are still unknown, a link has been recently suggested between the reduction of dopaminergic drugs (DA) (made possible by the benefits on the motor ability of deep brain stimulation) and the resurgence of the apathetic syndrome in these stimulated patients. In a first set of experiments, we set out to determine the role of the DA system in the emergence of such neuropsychiatric symptoms and which part of the DA ascending pathway is more specifically involved. Our lesion model in rats, by neurotoxic partial, selective and bilateral lesions of different regions of the DA midbrain continuum were performed allowed us to highlight a key role of the nigrostriatal DA pathway in the motivational processes and in regulating depressive- and anxiety-like behaviours, while avoiding motor impairments. In the second part, a pharmacological approach by chronic treatment with L-DOPA or Ropinirole (D2/D3 agonist) allowed us to verify the predictive value of our animal model in regard to treatment classically used in clinic. The administration of different selective agonists of the D1, D2 and D3 DA receptors has allowed us to show the major involvement of the D3 receptors in the efficiency to reverse the phenotype induced by the nigrostriatal pathway lesion, which opens the way for new therapeutic targets. Finally, the data obtained during this doctoral work provides new arguments for an involvement of the nigrostriatal DA pathway in the emergence of the apathetic syndrome in PD. The lesion model developed can lead to a better understanding of the role of DA in the processes underlying these motivational and mood disorders in PD and to identify new therapeutic strategies, more suitable for further treatment.SAVOIE-SCD - Bib.électronique (730659901) / SudocGRENOBLE1/INP-Bib.électronique (384210012) / SudocGRENOBLE2/3-Bib.électronique (384219901) / SudocSudocFranceF
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