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Electroconvulsive therapy (ECT) is based on conducting an electrical current through the brain to stimulate it and trigger generalized convulsion activity with therapeutic ends. Due to the efficient use of ECT during the last years, interest in the molecular bases involved in its mechanism of action has increased. Therefore, different hypotheses have emerged. In this context, the goal of this review is to describe the neurobiological, endocrine, and immune mechanisms involved in ECT and to detail its clinical efficacy in different psychiatric pathologies. This is a narrative review in which an extensive literature search was performed on the Scopus, Embase, PubMed, ISI Web of Science, and Google Scholar databases from inception to February 2022. The terms "electroconvulsive therapy", "neurobiological effects of electroconvulsive therapy", "molecular mechanisms in electroconvulsive therapy", and "psychiatric disorders" were among the keywords used in the search. The mechanisms of action of ECT include neurobiological function modifications and endocrine and immune changes that take place after ECT. Among these, the decrease in neural network hyperconnectivity, neuroinflammation reduction, neurogenesis promotion, modulation of different monoaminergic systems, and hypothalamus-hypophysis-adrenal and hypothalamus-hypophysis-thyroid axes normalization have been described. The majority of these elements are physiopathological components and therapeutic targets in different mental illnesses. Likewise, the use of ECT has recently expanded, with evidence of its use for other pathologies, such as Parkinson's disease psychosis, malignant neuroleptic syndrome, post-traumatic stress disorder, and obsessive-compulsive disorder. In conclusion, there is sufficient evidence to support the efficacy of ECT in the treatment of different psychiatric disorders, potentially through immune, endocrine, and neurobiological systems.

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Resumo Fundamento Alterações do substrato elétrico e anatômico do coração são fatores que originam e perpetuam a fibrilação atrial (FA), porém, os mecanismos envolvidos não foram totalmente elucidados ainda. Objetivo: Avaliar o papel do remodelamento do sistema nervoso cardíaco intrínseco (SNCI), incluindo fibras nervosas e receptores muscarínicos e β-adrenérgicos, na FA permanente humana. Métodos Foram avaliadas 4 amostras em átrios de 13 corações obtidos em necrópsias de pacientes com doença cardíaca e FA permanente, e em 13 controles com as mesmas doenças, porém, sem FA. Utilizando imunoperoxidase e histomorfometria, quantificamos a densidade das fibras do SNCI, bem como a porcentagem positiva de miocárdio para receptores β-adrenérgicos 1, 2 e 3, receptor quinase 5 acoplado à proteína G (GRK-5), e receptores muscarínicos 1 a 5. Os resultados foram comparados usando ANOVA e ANOVA hierarquizada e ajustados pelo volume do átrio esquerdo e, para avaliação da expressão de receptores β e GRK-5, pelo uso de β-bloqueadores. Adotamos como significativo α = 0,05. Resultados Houve aumento na densidade das fibras ( p <0,01), especialmente nas fibras simpáticas ( p =0,02). Quanto aos receptores muscarínicos, só houve diferença nos M1, que estavam aumentados (5,87±4,52 vs 2,85±2,40; p =0,03). Quanto aos componentes do sistema adrenérgicos analisados, houve expressão aumentada de β-3 (37,41 vs 34,18, p =0,04) e GRK-5 (51,16 vs 47,66; p<0,01). O uso de β-bloqueadores não teve impacto na expressão de receptores beta. Conclusão O aumento na inervação do SNCI e a alteração na expressão de receptores em regiões suscetíveis de desencadear FA podem ter um papel na fibrilação atrial permanente.

Abstract Background The primary factors that originate and perpetuate atrial fibrillation (AF) are electrical and anatomical substrate alterations. However, the central mechanisms governing AF perpetuation have not been elucidated yet, which is reflected on the modest results of the treatment in patients with long persistent AF. Objective To evaluate if human intrinsic cardiac autonomic nervous system (ICANS) remodeling, including nervous system fibers and muscarinic and β-adrenergic receptors, play a role in permanent AF. Methods Heart necropsy samples from thirteen patients with heart disease and permanent AF and thirteen controls without AF were used. By using immunoperoxidase and histomorphometry quantification, we identified the following: the density of all fibers of the ICANS, sympathetic and parasympathetic fibers; and the percentage of myocardium positive for β-adrenergic receptors 1, 2 and 3; G protein-coupled receptor kinase-5 (GRK-5); and muscarinic receptors M1 to M5. The results were compared using ANOVA and nested ANOVA and were adjusted according to the left atrium volume for all variables, and β-blocker use to evaluate the expression of β-receptors and GRK-5. Results There was an overall increase in the density of fibers of the ICANS (p=0.006), especially in atrial sympathetic nerve fibers (p=0.017). Only M1 muscarinic receptors were increased (5.87 vs 2.35, p=0.032). For adrenergic receptors, the results were positive for increased expression of β-3 (37.41 vs 34.18, p=0.039) and GRK-5 (51.16 vs 47.66; p<0.001). β-blocker use had no impact on β-receptor expression. Conclusion Increased ICANS innervation and remodeling receptor expression in regions prone to triggering AF may play a role in permanent AF.

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Schizophrenia is a heterogeneous disorder of mental symptoms and alterations, characterized by presenting abnormal ideas and perceptions, in which the individual loses contact with reality as a result of a complex neuropsychological disorganization, which affects the affective, intellectual and behavioral functioning; as well as inducing a significant social dysfunction. The etiology of schizophrenia is extremely complex, and is not very clear yet; it is believed to be the result of the combination of genetic factors and the environment. Numerous neurotransmitters have been implicated in this disease, as is the case of dopamine, serotonin and glutamate. The role of the inflammatory process in the pathogenesis of schizophrenia has been postulated, where a prenatal immune "challenge" during the second trimester of pregnancy can be key to the development of the disease. Some of the pro-inflammatory cytokines (TNF-alpha, IL-1beta and IL-6) play a key role in the processes of modulation of the nervous system functions related to affective, emotional and social alterations in subjects with schizophrenia. The mechanisms associated with inflammation and the anti-inflammatory defense system that may be associated with the development of schizophrenia are still unknown. This review was intended to address schizophrenia, in regards to the mechanisms associated with inflammation and the anti-inflammatory defense system in its development.

La esquizofrenia es un trastorno heterogéneo de síntomas y alteraciones mentales, caracterizadas por presentar ideas y percepciones anormales, en el que el individuo pierde contacto con la realidad a consecuencia de una compleja desorganización neuropsicológica, lo cual afecta el funcionamiento afectivo, intelectual y de comportamiento; asimismo, conlleva una disfunción social significativa. La etiología de la esquizofrenia aún no está establecida con claridad. Numerosos neurotransmisores han sido implicados en esta enfermedad, como es el caso de la dopamina, la serotonina y el glutamato. Se ha postulado el papel del proceso inflamatorio en la patogenia de la esquizofrenia, donde un "desafío" inmune prenatal durante el segundo trimestre de la gestación puede ser clave para el desarrollo de la enfermedad. Algunas de las citocinas proinflamatorias (TNF-alfa, IL-1beta e IL-6) juegan un papel clave en los procesos de modulación de las funciones del sistema nervioso relacionadas con alteraciones afectivas, emocionales y sociales en los sujetos con esquizofrenia. Aún se desconocen los mecanismos asociados con la inflamación y el sistema de defensa antiinflamatorio que pudieran intervenir en el desarrollo de la esquizofrenia. Esta revisión tuvo el propósito de tratar sobre la esquizofrenia, en lo que respecta a los mecanismos asociados con la inflamación y el sistema de defensa antiinflamatorio en su desarrollo.

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Resumen El trastorno depresivo mayor es una enfermedad que se caracteriza por la presencia de diferentes síntomas, que van desde no poder comer o dormir, hasta el no disfrute de las actividades que antes resultaban placenteras, ideas de minusvalía y suicidio. Las investigaciones del campo de las neurociencias y de las enfermedades psiquiátricas en especial, tienden cada vez más a buscar los posibles orígenes genéticos que expliquen su desarrollo y progresión. En esta revisión de la literatura se presenta lo reportado en estudios que no solo describen la enfermedad desde los trastornos neurofisiológicos, sino también desde alteraciones genéticas y epigenéticas, con el fin de brindar un mayor entendimiento de las bases moleculares y fisiopatológicas de esta patología psiquiátrica.

Abstract Major depressive disorder is a disease that is characterized by the presence of different symptoms, ranging from not being able to eat or sleep, to not enjoy activities that were previously pleasurable, ideas of disability and suicide. Research in the field of neurosciences and psychiatric diseases in particular, increasingly tend to seek the possible genetic origins that explain the development and progression of them. In this review of the literature, is presented what has been reported in studies, that not only describe the disease from its neurophysiological disorders, but also from the genetic and epigenetic alterations, in order to provide a better understanding of the molecular and physiopathological bases of this psychiatric pathology.

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Resumen El tabaquismo es factor de riesgo y a la vez una adicción compleja con componentes físicos, psicológicos y sociales. Adicción es la necesidad compulsiva de volver a consumir una droga para experimentar sus efectos, en el caso la nicotina, estimulación, euforia, placer, aumento de la atención concentración y memoria, además de disminución de la ansiedad, estrés y apetito. El Manual Diagnóstico y Estadístico de los Trastornos Mentales (DSM V) cataloga el tabaquismo como una adicción, la nicotina es una de las drogas más adictivas que existen, junto con la cocaína y la heroína, además demora 10 segundos en llegar al cerebro cuando se fuma. La nicotina se relaciona con distintos sistemas de neurotransmisión en el sistema nervioso central, es agonista de los receptores α4β2 de acetilcolina, siendo la unión receptor- neurotransmisor de alta sensibilidad. Las vías neurofisiológicas más importes implicadas en la dependencia por la nicotina son dopaminérgica (la más importante), noradrenérgica, GABA-érgica, glutamatérgica y endocanabinoide. El síndrome de abstinencia es una característica básica de la adicción, y es un conjunto de síntomas y signos, físicos y psíquicos que aparecen como consecuencia de la interrupción, reducción o abandono del tabaco. El síndrome de abstinencia se produce como consecuencia de varios factores: disminución de los niveles de cortisol plasmáticos, disminución de los niveles de noradrenalina en el Locus Coeruleous (LC) y principalmente disminución de los niveles de dopamina en el Núcleo Accumbens.

Smoking is a risk factor and at the same time a complex addiction with physical, psychological and social components. Addiction is the compulsive need to re-consume a drug to experience its effects, in the case of nicotine, stimulation, euphoria, pleasure, increased attention concentration and memory, plus decreased anxiety, stress and appetite. The Diagnostic and Statistical Manual of Mental Disorders (DSM V) lists smoking as an addiction, nicotine is one of the most addictive existing drugs, along with cocaine and heroin, and it takes 10 seconds to reach the brain when people smokes. Nicotine is related to different neurotransmission systems in the central nervous system, it is an agonist of acetylcholine α4β2 receptors, being the receptor-neurotransmitter junction of high sensitivity. The most important neurophysiological pathways involved in nicotine dependence are dopaminergic (most important), noradrenergic, GABA-ergic, glutamatergic and endocannabinoid. Abstinence syndrome is a basic characteristic of addiction, and is a set of physical and psychological symptoms and signs that appear because of interruption, reduction, or smoking cessation. Abstinence syndrome occurs as a consequence of several factors: decreased plasma cortisol levels, decreased levels of noradrenaline in the Locus Coeruleous and mainly decreased dopamine levels in Nucleous Accumbens.

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Contexto: O número de usuários de drogas ilícitas é estimado globalmente em 210 milhões de pessoas ao ano, das quais pelo menos 200.000 morrem em decorrência do uso. O consumo de drogas afeta não apenas o usuário, mas também a família, os amigos, os colegas de trabalho e a comunidade. Objetivo: O presente estudo traçou um perfil sociodemográfico de trabalhadores em tratamento para recuperação da dependência química na região de Campinas (SP). Método: Estudo transversal exploratório com dados colhidos por meio de questionário autoaplicado e anônimo em centros de recuperação para tratamento de dependência química no município de Campinas. A pesquisa foi conduzida entre julho de 2011 e julho de 2012 e analisou as condições de saúde e trabalho. A população estudada constituía-se de trabalhadores que estiveram em acompanhamento por mais de 30 dias, totalizando 200 pessoas. Resultados: A faixa etária de 18 a 54 anos representou 87,8% da amostra, com predominância de participantes com ensino médio completo e que desenvolviam alguma atividade remunerada, sendo que 54,5% estavam empregados formalmente, 48,4% com contratos inferiores a um ano, e 42,1% com faixa salarial abaixo de R$ 1.020,00. Conclusão: Este estudo apresenta informações pouco exploradas em outras pesquisas e com potencial para aprimorar as intervenções relacionadas à prevenção, ao tratamento e à reabilitação de trabalhadores em situação semelhante.

Context: The number of illicit drug users is estimated at 210 million people a year worldwide, of which at least 200,000 die as a consequence of the use. Drug use affects not only the user but also the family, friends, coworkers, and the community. Objective: This study outlines a sociodemographic profile of workers undergoing treatment for chemical dependency recovery in Campinas (SP). Method: Cross-sectional, exploratory study with data collected in rehabilitation centers for chemical dependency treatment in Campinas by means of a self-administered and anonymous questionnaire. The research was conducted between July 2011 and July 2012 and focused on the analysis of health and work conditions. The study included workers who were followed up for more than 30 days (n=200). Results: 87.8% of the population were aged 18­54 years, most of them had completed high school, had a remunerated activity, and of which 54.5% were formally employed, 48.4% with less than one year contracts and 42.1% with salary range below R$1,020.00 (Brazilian real). Conclusion: This study provides information not explored in other researches and has a potential value related to the prevention, treatment, and rehabilitation of workers in similar conditions.

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Background: Tourette syndrome is a neuropsychiatric disorder characterized by motor and vocal tics, attentional deficit, poor control of impulses and obsessive compulsive disorder. Pharmacological treatment is often disappointing due to partial response and frequent poor tolerance to neuroleptic drugs which are otherwise the most effective therapy so far. Aim: To report a lasting improvement obtained with a new drug, aripiprazole that acts modulating both dopaminergic and serotoninergic neurotransmission. Material and methods: Ten patients refractory to their usual therapy, aged 10 to 35 years, were switched to aripiprazole in an open trial. Results: Nine of the 10 patients showed a significant response assessed by the Yale severity tics rating scale and the clinical global impression scale (p <0.01). No relevant adverse effects were observed. Conclusions: Aripiprazole may be a good pharmacological option for patients with Tourette syndrome.

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