O córtex pré-frontal (PFC) participa do controle do comportamento de busca por droga e se projeta para a coluna rostrolateral da substância cinzenta periaquedutal (PAGrl) que por sua vez se projeta para o sistema orexinérgico da área hipotalâmica lateral (LHA) que controla comportamentos que oferecem recompensa através de projeções para o sistema dopaminérgico mesolímbico. O objetivo do trabalho é investigar a participação da PAGrl e a sua relação com o PFC e com o sistema orexinérgico da LHA na expressão do comportamento de busca por droga. Submetemos ratos Wistar ao condicionamento de preferência por lugar para sulfato de morfina e notamos que o PFC, a PAGrl e a LHA estão ativados em animais que expressaram tal comportamento. Após, realizamos lesões neuroquímicas bilaterais no PFC e notamos a ausência da busca pela droga nestes animais e da diminuição da ativação da PAGrl e do sistema orexinérgico da LHA. Posteriormente realizarmos lesões neuroquímicas por NMDA na PAGrl e notamos a ausência do comportamento e diminuição de duplas marcações para Fos e orexina na LHA. Os resultados indicam que a PAGrl exerceria um papel crítico para o comportamento de busca por droga, integrando aferências provenientes do PFC para modular os neurônios orexinérgicos da LHA. / The prefrontal cortex (PFC) is involved with planning of the drug seeking behavior and projects itself to the rostrolateral periaqueductal gray (PAGrl) that through projections for the orexin neurons in the lateral hypothalamic area (LHA), participates in the control of behavior that offer rewards. The LHA controls drug reward through projections for the mesolimbic dopaminergic system. This study aims to investigate the relationship between the PFC, PAGrl and orexin neurons in the LHA in drug seeking behavior. We did a morphine conditioned place preference (CPP) procedure in intact, bilateral PAGrl-lesioned and bilateral PFC-lesioned Wistar rats and investigated the pattern of Fos expression. The intact animals displayed such behavior and presented an increase in Fos activation in the PFC, rlPAG and LHA orexinergic neurons. Conversely, PAGrl-lesioned and PFC-lesioned animals did not display this behavior and reduced the activation of orexin neurons in the LHA. PFC-lesioned animals presented a reduction of the Fos activation in the rlPAG. The results suggest a pathway involving the PFC, PAGrl and LHA orexinergic cell group underlying the CCP, where the rlPAG would integrate inputs from the PFC to control the LHA orexinergic cell group.

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / ConvulsÃes e morte sÃo as principais conseqÃÃncias relacionadas à overdose de cocaÃna (COC). Para determinar os sistemas neurotransmissores envolvidos com as convulsÃes induzidas pela droga camundongos Swiss machos (20-30 g), foram prÃ-tratados (i.p.) 15, 30 ou 60 min antes da administraÃÃo de COC 90 mg/kg com drogas que interferem com vÃrios sistemas de neurotransmissÃo, observados por 30 min e avaliados quanto à latÃncia para o inÃcio da primeira convulsÃo, percentagem de animais que convulsionaram e percentagem de animais que sobreviveram ao tratamento. Dentre as drogas estudadas as GABAÃrgicas (diazepam, fenobarbital e gabapentina) apresentaram melhor resultado, aumentando a latÃncia para o inÃcio da primeira convulsÃo, reduzindo a percentagem de convulsÃes e morte. Das drogas dopaminÃrgicas, o antagonista do receptor D1, SCH23390, melhorou os 3 parÃmetros avaliados, enquanto o antagonista D2 pimozide reduziu a latÃncia. O antagonista muscarÃnico M1, pirenzepina, reduziu a percentagem de animais que convulsionaram. A fluoxetina, um inibidor da recaptaÃÃo da 5HT, reduziu a latÃncia das convulsÃes e a sobrevivÃncia, o mesmo acontecendo com o antagonista do receptor 5HT2, mianserina. A buspirona, agonista parcial do receptor 5HT1A, aumentou a sobrevivÃncia dos animais na menor dose estudada (5 mg/kg). O NMDA reduziu a latÃncia e a sobrevivÃncia dos animais, enquanto a cetamina, antagonista NMDA melhorou os trÃs parÃmetros estudados. Uma reduÃÃo na percentagem de animais que convulsionaram foi vista com o lÃtio, enquanto a vitamina E reduziu a percentagem de animais que convulsionaram e aumentou a percentagem de sobrevivÃncia. O antagonista opiÃide naltrexone reduziu a latÃncia e aumentou a morte. Observou-se que apÃs a overdose de COC alguns animais apresentaram estado de mal epilÃptico (EME), enquanto outros morreram apÃs as convulsÃes. Assim, para a realizaÃÃo dos estudos neuroquÃmicos estes animais foram dissecados para retirada do corpo estriado (CE) e cÃrtex prÃ-frontal (CPF) e divididos em dois grupos, EME e morte. ApÃs EME ocorreu uma reduÃÃo (40 %) e aumento (125 %) nos nÃveis de dopamina (DA), respectivamente em CE e CPF, havendo tambÃm um aumento nos metabÃlitos DOPAC e HVA, respectivamente em CPF e CE. ApÃs a morte os nÃveis de DA reduziram (38 %) em CPF e ambos os metabÃlitos aumentaram em CE. As taxas metabÃlicas para esta monoamina aumentaram apÃs EME no CE e apÃs a morte no CE e CPF. O aumento no metabolismo da DA està relacionado à formaÃÃo de radicais livres. A 5HT aumentou (123 %) apenas no CPF apÃs EME, enquanto seu metabÃlito 5HIAA reduziu no CPF apÃs EME e morte induzida por cocaÃna. A taxa metabÃlica da 5HT reduziu apÃs EME no CPF e apÃs a morte em ambas as Ãreas estudadas. A NA no EME diminuiu (52 %) no CE e aumentou (56 %) no CPF, enquanto na morte aumentou no CE e reduziu em CPF. O EME promoveu reduÃÃo (46 %) no nÃmero de receptores D1-sÃmile em CE e CPF. Esta reduÃÃo foi acompanhada por uma reduÃÃo e aumento, respectivamente da afinidade (Kd) do receptor pelo ligante radioativo. Tanto EME como morte aumentaram (48 % em CPF e 82 % no CE) o nÃmero de receptores D2-sÃmile, com aumento na afinidade no CPF e reduÃÃo no CE. Os receptores M1-sÃmile reduziram no CPF apÃs EME e morte induzida por COC. A atividade da AChE aumentou apÃs EME (CE) e apÃs a morte (CE e CPF). Os receptores 5HT2 aumentaram (em torno de 46 e 460 %, respectivamente, no CPF e CE) apÃs EME e morte. Os receptores GABAÃrgicos e glutamatÃrgicos apresentaram a mesma alteraÃÃo, com reduÃÃo do nÃmero apÃs EME nas duas Ãreas estudadas, e na morte apenas no CPF. Os nÃveis de nitrito/nitrato aumentaram em ambas condiÃÃes experimentais e Ãreas cerebrais que no caso dos receptores GABAÃrgicos e glutamatÃrgicos. Os nÃveis de MDA aumentaram (46 %) no CE apÃs a morte induzida por cocaÃna. Das enzimas antioxidantes a catalase teve sua atividade reduzida pela overdose de COC no CPF e CE e pela COC em baixas doses (10 e 30 mg/kg) apenas no CE. O prÃ-tratamento com diazepam levou a catalase para nÃveis controle. A glutationa reduzida (GSH) aumentou apÃs a morte no CE e CPF. Os resultados mostram que as convulsÃes e morte induzidas por cocaÃna sÃo eventos multimediados e que as Ãreas cerebrais estudadas, CPF e CE tÃm uma importante participaÃÃo neste processo. O estresse oxidativo tambÃm parece estar envolvido neste mecanismo. Estes achados podem ser importantes para a determinaÃÃo de um mecanismo neural para a toxicidade aguda induzida pela cocaÃna. / Seizures and death are the most important toxic consequences related to cocaine (COC) overdose. In order to determine the main neurotransmitter systems involved with cocaine-induced seizures, male Swiss mice (20-30 g) were pretreated (i.p.) 15, 30 or 60 min before COC 90 mg/kg administration with drugs that interferes with various neurotransmitter systems. The animals were observed (30 min) to determine: latency to first seizure, number of seizures, and number of deaths after cocaine overdose. Gabaergic drugs (diazepam, Phenobarbital and gabapentin) were the best ones, increasing latency to 1st seizure and decreasing cocaine-induced seizures and mortality. The D1 receptor antagonist SCH23390 improved the three parameters observed, while the D2 antagonist pimozide (20 mg/kg) decreased latency. Pirenzepine, a M1 receptor antagonist decreased the number of animals that seized. Fluoxetine, an inhibitor of serotonin reuptake, decreased latency to 1st seizure and survival, and the same happened with mianserin, a 5-HT2 receptor antagonist. Buspirone, a partial agonist of 5HT1A receptor increased animals survival, while ketamine, a NMDA receptor antagonist improved all three parameters evaluated. Lithium decreased the number of animals that seized, while vitamin E decreased the number of animals that seized and also mortality. The opioid antagonist naltrexone, decreased latency and increased cocaine-induced death. It was observed that after cocaine overdose some animals presented only status epilepticus (SE), while others died after seizures. Thus, for neurochemical studies these animals were dissected, striatum (ST) and prefrontal cortex (PFC) removed, and divided in two groups, SE and death. SE decreased (40 %) and increased (125 %) DA levels in ST and PFC, respectively. There was also an increase in DA metabolites, DOPAC and HVA in PFC and ST, respectively. After death, DA levels decreased (38%) in PFC and both metabolites increased in ST. Metabolic rates for this monoamine increased after SE in ST and after death in ST and PFC. The increase in DA metabolism is related to free radicals formation. 5HT increased (123 %) only in PFC after SE, while its metabolite 5HIAA decreased in PFC after SE and death induced by cocaine. The metabolic rate for 5HT decreased after SE in PFC and after death in both areas studied. NA decreased (52 %) in ST and increased (56 %) in PFC during SE, while after death increased in ST and decreased in PFC. Dopaminergic D1-like receptors decreased (46 %) in ST and PFC after SE. This reduction was followed by a decrease and increase, respectively, of the affinity (Kd) receptor-radioactive ligand. An increase (48 % in PFC and 82 % in ST) in D2-like receptors number was observed and followed by an increase in affinity in PFC and decrease in ST. Muscarinic M1 receptors decreased in PFC after cocaine-induced SE and death. AChE activity increased after SE (ST) and after death (ST and PFC). Serotonergic 5HT2 receptors increased (around 46 % and 460 %, respectively to PFC and ST) after SE and death. GABAergic and glutamatergic receptors presentes the same alterations, reduction after SE in both brain areas studied and only in PFC after death. Nitrite/nitrate levels increased in all conditions determined for GABAergic and glutamatergic receptors. MDA levels increased (46 %) only after death in ST. From antioxidant enzymes, catalase had its activity decreased after cocaine overdose in ST and PFC, the same happened with cocaine in low doses (10 and 30 mg/kg), only in ST. Pretreatment with diazepam brought catalase levels to control values. Glutathione increased after death in ST and PFC. Taken together these results showed that cocaine-induced seizures and death are multimediated events and that the brain areas studied, PFC and ST are important to this brain process. Oxidative stress also seems to be involved in this mechanism. These findings may be important for determining the neural mechanisms that mediate acute cocaine toxicity.

Les hallucinations auditives (HA) sont présentes chez 70% à 80% des patients atteints de schizophrénie et sont résistantes aux traitements pharmacologiques dans environs 25% cas. Ces symptômes induisent une détresse importante chez les sujets et grèvent le pronostic. Dans ce travail, nous avons mis en avant des altérations cérébrales spécifiques aux HA chez des patients atteints de schizophrénie. Dans une première étude, en utilisant la méthode de DTI, nous avons montré que les patients atteints de schizophrénie avec HA ont une intégrité du faisceau arqué, supérieure à celle mesurée chez des patients atteints de schizophrénie sans HA. Dans une seconde étude, en utilisant la méthode de SRM, nous avons montré une augmentation de NAA, reflet du métabolisme neuronal, dans le cortex préfrontal dorsolatéral de l'hémisphère droit chez les patients atteints de schizophrénie avec HA comparé au CPFDL gauche et à des patients atteints de schizophrénie sans HA. Dans ces deux études, le taux de NAA du CPFDL droit et l'intégrité du faisceau arqué ont été associés à la sévérité des HA présentes chez les patients. Dans notre dernière étude, nous avons montré une association entre le taux de BDNF périphérique, marqueur de la plasticité neuronale, et le taux de NAA mesuré dans le CPFDL droit, chez les patients atteints de schizophrénie résistante. Ces résultats montrent qu'il existe une pathophysiologie spécifique des HA chez les patients atteints de schizophrénie et mettent en avant l'importance de stratifier les patients sur la base de leurs symptômes prédominants dans les futures études pathophysiologiques de la schizophrénie / Auditory hallucinations (AH) are present in 70% to 80% of patients with schizophrenia and are resistant to pharmacological treatments in 25% of cases. These symptoms induce significant distress in patients and predict a bad prognosis. In this work we have highlighted cerebral alterations specific to AH in patients suffer from schizophrenia. In a first study, using DTI method, we showed that patients with schizophrenia and AH have an arcuate fasciculus integrity, reflected by the measurement of fractional anisotropy (FA) greater than the one measured in patients with schizophrenia without AH. In a second study, using MRS method, we showed an increase of NAA level measured in the dorsolateral prefrontal cortex (DLPFC) in the right hemisphere in patients with schizophrenia and AH compared to the DLPFC in the left hemisphere and compared to patients with schizophrenia and without AH. Moreover, in these two studies we showed an association between AH severity and the arcuate fasciculus integrity in the left hemisphere and an association between AH severity and NAA levels in the right DLPFC. Finally, in our last study, we quantified BDNF levels using ELISA method and showed an association between peripheral BDNF level, a marker of neuronal plasticity, and NAA levels in the right DLPFC, marker of neuronal metabolism, in patients with treatment-resistant schizophrenia. These results show that there is a specific pathophysiology of AH in patients with schizophrenia and highlight the importance of stratifying patients on the basis of their predominant symptoms in future pathophysiological studies of schizophrenia

No description available.

L’apprentissage social améliore les performances non seulement chez l’homme et les primates non humains, mais aussi chez un grand nombre d’espèces. Chez le singe, les corrélats neuronaux de l’apprentissage individuel sont parfaitement connus, mais ceux de l’apprentissage social font cependant défaut, en partie à cause des conditions dans lesquelles il a été étudié, jusqu’à maintenant et qui n’étaient pas compatibles avec les enregistrements neuronaux. Ce travail aborde deux questions d’actualité : Les singes peuvent-ils apprendre par observation dans les conditions contraignantes de l’électrophysiologie ? L’apprentissage social est-il médié par les mêmes mécanismes et circuits cérébraux que l’apprentissage individuel par renforcement ? Nos résultats ont montré que les singes apprennent plus rapidement de l’expérience du model que de leur propre expérience, et que le bénéfice est plus important après observation des erreurs que des succès. L’activité neuronale du cortex préfrontal est modulée de façon parallèle aux résultats comportementaux. Nous proposons que l’apprentissage associatif, qu’il soit basé sur l’expérience individuelle ou celle d’autrui, implique les mêmes réseaux cérébraux incluant les cortex préfrontal, et qu’il est probablement médié par les mêmes mécanismes neuronaux de la prédiction de l’erreur durant l’apprentissage par renforcement. / Social learning improves the performance not only in humans and non-human primates, but in a host of animal species as well. In monkeys, the neuronal correlates of individual learning are well understood, but those of social learning are lacking partly because it has been addressed, so far, in conditions not compatible with neuronal recordings. Do monkeys learn by observation under the constraining conditions of electrophysiology? Is social learning mediated by the same brain circuits and mechanisms as individual, reinforcement based learning? This work addressed these two timely questions. Our findings showed that monkeys learn faster from the model’s experience than from their own experience, and that they benefit more from observed errors than from successes. Neuronal processing of observed errors in the prefrontal cortex parallels this behavioral result. We suggest that associative learning, whether based on individual or others’ experience, involves the same brain networks including prefrontal cortex, and is probably mediated by the same neuronal mechanisms of error prediction during reinforcement-based learning.

La pathogénèse de désordres psychiatriques comme les troubles de l'humeur et la schizophrénie met en jeu des facteurs génétiques et environnementaux. La reelin, une protéine de la matrice extracellulaire et l'isolement social (IS), un stress environnemental participeraient à l'étiologie de ces maladies. Le cortex préfrontal (CPF) impliqué dans les fonctions cognitives et exécutives, présente des anomalies morpho-fonctionnelles chez les patients atteints de ces troubles. Le but de ma thèse est d'étudier l'effet de l'IS et d'une haplo-insuffisance en reelin (HIR) sur les propriétés du CPF adulte. Nous utilisons des souris hétérozygotes reelin et sauvages soumises à l'IS et procédons à une analyse électrophysiologique, morphologique et comportementale. Nos résultats montrent que l'IS induit des défauts de transmission et de plasticité synaptique et du comportement. Nous avons également montré que l'HIR aggrave ces défauts. Finalement, nous avons exploré une piste thérapeutique prometteuse. / The pathogenesis of psychiatric disorders such as mood disorders and schizophrenia involves genetic and environmental factors. The reelin, a protein of the extracellular matrix and social isolation (SI), an environmental stress participate in the etiology of these diseases. The prefrontal cortex (PFC) involved in cognitive and executive functions, exhibits morpho-functional abnormalities in patients with these disorders. The purpose of my thesis is to study the effect of the SI and a haploinsufficiency in reelin (HIR) on the properties of the adult PFC. We used wild mice and reelin heterozygous mice that underwent and proceed to electrophysiological, morphological and behavioral analyses. Our results show that the SI altered synaptic transmission and plasticity and behavior. We also showed that the HIR aggravates these alterations. Finally, we explored a promising therapy.

L’anxiété est un symptôme prédominant au cours des périodes initiales de sevrage à la cocaïne et est considérécomme un facteur important de rechute. Le but de cette étude était de caractériser les dysfonctionnementscérébraux qui pourraient contribuer à l’expression de cet état pathologique chez le rat.Les rats sont traités avec de la cocaïne en chronique et le comportement anxieux est évalué au cours du sevragedans différents paradigmes expérimentaux (tests du labyrinthe en croix surélevé, du confinement dans un brasouvert surélevé et de l’enfouissement défensif). Nos résultats ont montré que le sevrage à la cocaïne induit unétat anxieux élevé qui persiste pendant au moins 28 jours de sevrage. Nous avons ensuite utilisél’immunohistochimie de Fos pour comparer les patterns d’activation cérébrale chez les rats sevrés et témoinsaprès exposition au test de l’OA. Nos données ont montré que l’anxiété élevée des rats sevrés était accompagnéed’une altération de la réactivité des neurones glutamatergiques de la partie dorsale du cortex préfrontal médian(dCPFm) et de certaines régions sous-corticale (aires hypothalamiques latérale et antérieure et le noyauparaventriculaire du thalamus). Nous avons ensuite montré que l’inactivation pharmacologique du dCPFm avecdu muscimol atténuait les comportements anxieux des rats sevrés suggérant ainsi une hyperréactivité de cetterégion corticale durant le traitement des informations de type anxieux. Notre étude amène des données nouvellesquant aux substrats neuronaux sous-tendant l’anxiété pathologique observée au cours du sevrage à la cocaïne etsouligne l’importance du CPFm dans la régulation de cet état d’anxiété pathologique. / Anxiety is one of the prevailing symptoms observed during the initial period of abstinence in cocaine abusersand is considered as an important factor of relapse. The aim of this study was to provide further insight into thecerebral dysregulations that might contribute to this pathological state in rats.Rats were treated chronically with cocaine and anxiety-behaviors were assessed in different paradigms duringwithdrawal (elevated plus maze, open arm and shock probe burying tests). Our results demonstrated that cocainewithdrawal induced persistent heightened levels of anxiety that last for at least 28 days. We then used Fosimmunohistochemistry to map neuronal activation patterns in withdrawn rats confined to one open arm (OA) ofan elevated plus maze. Our data showed that the exacerbated anxiety observed in cocaine treated rats exposed toan OA was accompanied by an altered reactivity of the dorsal part of the medial prefrontal cortex (dmPFC)glutamatergic neurons and some sub-cortical regions (anterior and lateral hypothalamic areas and theparaventricular nucleus of the thalamus). Finally, we showed that pharmacological inactivation of the dmPFCwith muscimol considerably attenuated anxiety-related behaviors in cocaine withdrawn rats suggesting anexaggerated response of this cortical area during the processing of anxiogenic stimuli. The present studyprovides new data on the neural substrate underlying pathological anxiety observed during cocaine withdrawaland highlights the importance of the dmPFC in the regulation of this pathological anxiety state.

Submitted by Renata Lopes (renatasil82@gmail.com) on 2015-12-17T18:50:18Z No. of bitstreams: 1 mayarasilvadamata.pdf: 1134340 bytes, checksum: c4c65cefb5b2804563f056ccd867cdfe (MD5) / Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2016-01-25T15:09:09Z (GMT) No. of bitstreams: 1 mayarasilvadamata.pdf: 1134340 bytes, checksum: c4c65cefb5b2804563f056ccd867cdfe (MD5) / Made available in DSpace on 2016-01-25T15:09:09Z (GMT). No. of bitstreams: 1 mayarasilvadamata.pdf: 1134340 bytes, checksum: c4c65cefb5b2804563f056ccd867cdfe (MD5) Previous issue date: 2015-02-10 / O álcool elicia prejuízo em habilidades cognitivas, tais como as funções executivas (FE), que incluem vários constructos distinguíveis. Assim, o conhecimento dos efeitos agudos desta substância sobre os constructos das FE é necessário para melhor caracterizar seus potenciais efeitos cognitivos. Objetivo: Verificar os efeitos agudos do álcool no desempenho de seis constructos eleitos das funções executivas (alternância, atualização, inibição, eficiência do acesso à memória de longo prazo, planejamento, dupla tarefa) em jovens saudáveis. Metodologia: Foram recrutados 45 indivíduos do sexo masculino com idades entre 18 e 30 anos que eram bebedores sociais. Eles foram alocados aleatoriamente em três grupos de 15 participantes: um grupo cuja dose de álcool era de 0,6 g/kg de peso; outro de 1,0 g/kg de peso; e o grupo placebo. Resultados: Não foram detectadas diferenças significativas entre grupos nos testes executivos. Discussão: Foram determinados os tamanhos de amostras necessários para a observação de efeitos de álcool nesta população, que foram em geral bastante elevados. Conclusão: O presente estudo foi pioneiro no Brasil no âmbito proposto e encontrou magnitudes de efeito de relevância clínica para os constructos: alternância, fluência semântica, inibição e atualização. / Alcohol (ethanol) elicits impairment in cognitive abilities such as executive functions (EF), which includes various separable constructs. Thus, knowledge of the acute effects of this substance on the constructs of EF is necessary to better characterize its potential cognitive effects. Objective: To investigate the acute effects of alcohol on performance of six elected constructs of executive functions (shifting, updating, inhibition, access to long-term memory, planning, dual-tasking) in young healthy individuals. Methods: we recruited 45 male subjects aged between 18 and 30 years who were social drinkers. They were randomly allocated to three groups of 15 participants: one group whose alcohol dose was 0.6 g / kg; another group whose dose was 1.0 g / kg; and the placebo group. Results: No group significant differences were found in the executive tests. Discussion: It was determined the sample size necessary to monitor the effects of alcohol in this population were generally quite high. Conclusion: The present study was pioneer in Brazil in the proposed framework and found effect magnitudes of clinical relevance for the constructs: shifting, semantic fluency, inhibition and updating.

Submitted by Renata Lopes (renatasil82@gmail.com) on 2016-01-19T16:24:04Z No. of bitstreams: 1 julianealvarezdetoledo.pdf: 5687649 bytes, checksum: 089e1997adee1c910ab6e02c0cef5b85 (MD5) / Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2016-01-25T17:59:53Z (GMT) No. of bitstreams: 1 julianealvarezdetoledo.pdf: 5687649 bytes, checksum: 089e1997adee1c910ab6e02c0cef5b85 (MD5) / Made available in DSpace on 2016-01-25T17:59:53Z (GMT). No. of bitstreams: 1 julianealvarezdetoledo.pdf: 5687649 bytes, checksum: 089e1997adee1c910ab6e02c0cef5b85 (MD5) Previous issue date: 2014-11-28 / FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais / Introdução: O uso do etanol é mais comum entre os adultos jovens e é uma substância capaz de causar danos significativos ao SNC, afetando diretamente processos neuromaturacionais e consequentemente, habilidades cognitivas complexas, tais como as Funções Executivas (FE). Assim, o conhecimento dos efeitos agudos desta substância sobre os constructos das FE é necessário para traçar o perfil do funcionamento cognitivo, que pode vir a ser afetado pelo uso desta substância. Objetivo: Verificar os efeitos agudos do etanol no desempenho dos três constructos eleitos das funções executivas em estudantes universitários de Juiz de Fora que são usuários ocasionais de álcool. Metodologia: Foram recrutados 45 indivíduos do sexo masculino, com idades entre 18 e 30 anos, que foram submetidos aos testes para caracterização da amostra e em seguida, alocados aleatoriamente em três grupos de 15 participantes: um grupo cuja dose de etanol era de 0,6 mg/kg de peso; outro de 1,0 mg/kg de peso; e o grupo placebo; todas acrescidas à 300 ml de cerveja sem álcool gelada. Os testes específicos para avaliação dos constructos das FE. foram realizados próximo ao pico de absorção do etanol, cerca de 40 minutos após a ingestão. Resultados: Houve diferença entre grupos na medida do etilômetro pós-teste e os três grupos foram diferentes entre si. Não houve diferença significativa entre os resultados obtidos nos demais testes. Discussão: Os achados corroboram estudos prévios com administração de etanol em indivíduos humanos em que não foram encontrados efeitos agudos decorrentes do consumo de álcool sobre os constructos das FE. Conclusão: O presente estudo foi pioneiro no Brasil para avaliação de jovens universitários no âmbito proposto. Novos estudos são necessários, com maior número de participantes, de ambos os sexos, para a definição da dose de etanol que seja capaz de afetar as FE e de reproduzir resultados em laboratório. / Introduction: Ethanol use is more common among young adults and it`s a substance capable of causing significant damage to the central nervous system, affecting neuromaturational processes directly and consequently, complex cognitive abilities such as executive functions (EF). Thus, knowledge of the acute effects of this substance on the constructs of EF is necessary to profile the cognitive functioning, which may ultimately be affected by the use of this substance. Objective: To investigate the acute effects of ethanol on performance of three elected constructs of executive functions in university students of Juiz de Fora who are occasional users of alcohol. Methods: 45 male subjects, aged between 18 and 30 years who were tested to characterize the sample and then were randomly allocated into three groups of 15 participants: one group whose ethanol dose was 0.6 mg / kg; another group whose dose was 1.0 mg / kg; and the placebo group; all of it was added to 300 ml of chilled alcohol free beer. The specific tests to evaluate the components of EF were performed near the peak absorption of ethanol, about 40 minutes after ingestion. Results: There were differences between groups in the extent of post-breathalyzer test and the three groups were different. There was no significant difference between the results obtained in the other tests. Discussion: These findings corroborate to previous studies with administration of ethanol in human subjects in which no acute effects of consuming alcohol on the constructs of EF were found. Conclusion: The present study was pioneer in Brazil for evaluation of university students in the proposed framework. Further studies are needed with larger numbers of participants, of both sexes, to define the dose of ethanol that is capable of affecting the FE and reproduce laboratory results.

No description available.