RESUMO
Background: The outbreak of coronavirus disease 19 has led to measures of social distancing and quarantine worldwide. This stressful period may lead to psychological problems, including changes in substance use. In addition, sociodemographic factors are linked to changed levels of drug use and abuse observed during the COVID-19 pandemic, which are also associated with increased anxiety, depression, and other disorders. Thus, the aim of the study was to investigate (i) changes in drug use during the COVID-19 pandemic associated with social distancing, and (ii) to verify factors associated with those changes. Methods: A web-based cross-sectional observational survey was completed by a self-selected adult general population in Brazil (N = 2,435) during September/October 2020 (first wave) before and throughout the pandemic. Key outcomes: social distancing, self-reported drug use (ASSIST), and emotional states (DASS-21). Results: High social distancing was associated with fewer chances (prevalence ratio) of increased drug use for alcohol (0.71, CI95%: 0.64-0.80), tobacco (0.72; CI95%: 0.60-0.87), cannabis (0.65; CI95%: 0.55-0.78), and others. Low social distancing presented a higher DASS-21 score for anxiety (P = 0.017). Concerning covariates analysis by a general linear model, men (alcohol: 1. 71; cannabis: 3.86), younger age (alcohol: 0.97), less education (alcohol, tobacco, cannabis and cocaine/crack comparing several lower schooling categories vs. higher education), lower income (alcohol: 0.42; tobacco: 0.47; and cannabis: 0.36), and higher depression DASS-21 score (alcohol: 1.05; tobacco: 1.08; cannabis: 1.07; and cocaine/crack: 1.07) were associated with higher use prevalence of several drugs. Conclusions: Individuals reporting low social distancing increased the use of most drugs during the pandemic, while high social distancing significantly decreased drug use. Anxiety and depressive states and several sociodemographic factors (men; lower income; less education) were associated with higher drug use patterns.
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BACKGROUND: The effects of tobacco smoke on the central nervous system are usually studied with isolated nicotine, ignoring other compounds present in cigarette smoke. The few studies that use in vivo whole-body cigarette smoke exposure are usually performed in expensive commercial apparatus. NEW METHOD: We presented a feasible, safe, and low-cost apparatus for cigarette smoke exposure in rodents. RESULTS: Rats exposed to cigarette smoke in this apparatus showed cotinine levels similar to human active smokers. Additional results showed that cigarette smoke exposure increased glutamate and aspartic acid levels and decreased leucine, isoleucine, ornithine, phenylalanine, and tryptophan levels in the cerebrospinal fluid of rats. COMPARISON WITH EXISTING METHOD(S): Our apparatus is feasible, safe, and costs 67-fold less than a commercial automatized smoking machine. Beyond the low cost, it does not require specialized knowledge for building or maintenance. CONCLUSIONS: We concluded that our low-cost apparatus is reliable and reproduces cigarette smoke use in humans.
Assuntos
Fumar Cigarros , Animais , Cotinina , Nicotina , Ratos , NicotianaRESUMO
Copaiba oleoresin, extracted from the Copaifera reticulata tree, has been used as a remedy in popular medicine in the Brazilian Amazon for various purposes, including reducing drug abuse. Yet no studies evaluated the effect of repeated administration of copaiba oil on alcohol consumption in animals. To evaluate this effect, we divided adult male Wistar rats into a) an alcohol group in which the animals had free access to choose between two bottles: one containing alcohol solution (20%) and another containing vehicle solution (0.2% saccharin); and b) a control group with access to two bottles containing vehicle solution. Rats were free to drink 24 h per day, for 35 days. Daily alcohol consumption and weekly body weight gain and food intake were monitored. From day 22, half of the rats in each group received 600 mg kg-1 copaiba oleoresin and the other received vehicle, subcutaneously, once a day, for three days. On day 35, rats were evaluated in an open-field test. The results showed that copaiba oil decreased voluntary alcohol intake and preference between days 2 and 6 after the last administration. Copaiba treatment also decreased the food intake and body weight gain in both alcohol and control groups without changing behaviors in the open-field test. Therefore, copaiba oil was able to reduce voluntary alcohol consumption in rats and could be tested in humans as an adjuvant to treat alcohol use disorder.(AU)
O óleo extraído da árvore copaíba, Copaifera reticulata, tem sido usado na medicina popular na Amazônia brasileira para diversos fins, incluindo abuso de drogas. Contudo, não há estudos avaliando o efeito da administração repetida do óleo de copaíba sobre o consumo de álcool em animais. Para avaliar esse efeito, dividimos ratos Wistar machos adultos em dois grupos: a) um grupo álcool, no qual os animais tinham livre acesso a duas garrafas: uma contendo solução alcoólica (20%) e outra contendo solução veículo (sacarina 0,2%); e b) um grupo controle com acesso a duas garrafas contendo solução veículo. Os ratos podiam beber livremente, 24 horas por dia, durante 35 dias. O consumo diário de álcool, bem como o ganho de peso corporal semanal e a ingestão de alimentos foram monitorados. A partir do dia 22, metade dos ratos de cada grupo recebeu 600 mg kg-1 de óleo de copaíba e a outra metade recebeu veículo, por via subcutânea, uma vez ao dia, durante três dias. No dia 35, os ratos foram testados em teste de campo aberto. Os resultados mostraram que o óleo de copaíba diminuiu a ingestão voluntária e a preferência por álcool entre os dias 2 e 6 após a última administração. O tratamento com óleo de copaíba também diminuiu a ingestão alimentar e o ganho de peso corporal em ambos os grupos álcool e controle, sem alterar o comportamento no teste de campo aberto. Portanto, o óleo de copaíba foi capaz de reduzir o consumo voluntário de álcool em ratos e poderia ser testado em humanos como um adjuvante para tratar transtorno de uso de álcool.(AU)
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Animais , Ratos , Consumo de Bebidas Alcoólicas/efeitos adversos , Óleos Voláteis , Produtos Biológicos , Fabaceae/químicaRESUMO
Allopregnanolone (3α,5α-tetrahydroprogesterone; pharmaceutical formulation: brexanolone) is a neurosteroid that has recently been approved for the treatment of postpartum depression, promising to fill part of a long-lasting gap in the effectiveness of pharmacotherapies for depressive disorders. In this review, we explore the experimental research that characterized the antidepressant-like effects of allopregnanolone, with a particular focus on the neurotrophic adaptations induced by this neurosteroid in preclinical studies. We demonstrate that there is a consistent decrease in allopregnanolone levels in limbic brain areas in rodents submitted to stress-induced models of depression, such as social isolation and chronic unpredictable stress. Further, both the drug-induced upregulation of allopregnanolone or its direct administration reduce depressive-like behaviors in models such as the forced swim test. The main drugs of interest that upregulate allopregnanolone levels are selective serotonin reuptake inhibitors (SSRIs), which present the neurosteroidogenic property even in lower, non-SSRI doses. Finally, we explore how these antidepressant-like behaviors are related to neurogenesis, particularly in the hippocampus. The protagonist in this mechanism is likely the brain-derived neurotrophic factor (BFNF), which is decreased in animal models of depression and may be restored by the normalization of allopregnanolone levels. The role of an interaction between GABA and the neurotrophic mechanisms needs to be further investigated.
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Interactions on neurotransmitter systems in the reward pathways may explain the high frequency of combined use of alcohol and cigarettes in humans. In this study, we evaluated some behavioral and neurochemical changes promoted by chronic exposure to alcohol and cigarette smoke in rats. Adult rats were administered with 2 g/kg alcohol (v.o.) or/and inhaled the smoke from 6 cigarettes, twice/day, for 30 days. Behavioral tests were performed 3 h after the alcohol administration and 1 h after the last exposure to cigarette smoke in the morning. Cerebrospinal fluid was collected for glutamate determination and the hippocampus was dissected for GABAA and NMDA receptor subunits mRNA expression determination. Results showed that the combined use of alcohol and cigarette smoke (ALTB) in rats increased the locomotor activity and all interventions decreased anxiety-like behaviors. Despite being on a short-term withdrawal, the cigarette smoke exposure decreased the percentage of open arm entries in the elevated plus maze test, which was prevented by combined use with alcohol. Even though GABAA and glutamate receptor subunits expression did not change in the hippocampus, glutamate levels were significantly higher in the cerebrospinal fluid from ALTB rats. Therefore, we showed that the combined use of alcohol and cigarette maintained a psychostimulant effect after a short-term withdrawal that was associated with the elevated glutamatergic activity. The combined use also prevented anxiety-like signs in cigarette smoke exposure rats, decreasing an adverse effect caused by nicotine withdrawal. These results could explain, in part, the elevated frequency of combined use of these two drugs of abuse in humans.
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Ansiedade/tratamento farmacológico , Comportamento Animal/efeitos dos fármacos , Depressores do Sistema Nervoso Central/farmacologia , Fumar Cigarros , Etanol/farmacologia , Ácido Glutâmico/líquido cefalorraquidiano , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Locomoção/efeitos dos fármacos , Receptores de GABA-A/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Animais , Depressores do Sistema Nervoso Central/administração & dosagem , Quimioterapia Combinada , Etanol/administração & dosagem , Ácido Glutâmico/efeitos dos fármacos , Aprendizagem em Labirinto , RNA Mensageiro , Ratos , Ratos Wistar , Receptores de GABA-A/efeitos dos fármacos , Receptores de N-Metil-D-Aspartato/efeitos dos fármacosRESUMO
There is increasing evidence suggesting that oxidative stress plays an important role in the development of many chronic and degenerative conditions such as diabetic encephalopathy and depression. Considering that diabetic rats and mice present higher depressive-like behaviour when submitted to the forced swimming test and that treatment with insulin and/or clonazepam is able to reverse the behavioural changes of the diabetic rats, the present work investigated the antioxidant status, specifically total antioxidant reactivity and antioxidant potential of insulin and clonazepam, as well as the effect of this drugs upon protein oxidative damage and reactive species formation in cortex, hippocampus and striatum from diabetic rats submitted to forced swimming test. It was verified that longer immobility time in diabetic rats and insulin plus clonazepam treatment reversed this depressive-like behaviour. Moreover, data obtained in this study allowed to demonstrate through different parameters such as protein carbonyl content, 2'7'-dichlorofluorescein oxidation, catalase, superoxide dismutase, glutathione peroxidase assay, total radical-trapping antioxidant potential and total antioxidant reactivity that there is oxidative stress in cortex, hippocampus and striatum from diabetic rats under depressive-like behaviour and highlight the insulin and/or clonazepam effect in these different brain areas, restoring antioxidant status and protein damage.
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Anticonvulsivantes/uso terapêutico , Encefalopatias/complicações , Clonazepam/uso terapêutico , Depressão/tratamento farmacológico , Diabetes Mellitus Experimental/complicações , Hipoglicemiantes/uso terapêutico , Insulina/uso terapêutico , Animais , Antioxidantes/metabolismo , Córtex Cerebral/metabolismo , Córtex Cerebral/patologia , Corpo Estriado/metabolismo , Corpo Estriado/patologia , Depressão/etiologia , Hipocampo/metabolismo , Hipocampo/patologia , Masculino , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismoRESUMO
CONTEXT: It is known that oxidative stress occurs in peripheral blood in an experimental animal model of diabetes and depression, and acute treatment with insulin and clonazepam (CNZ) has a protective effect on oxidative stress in this model. OBJECTIVE: This study evaluated the effect of insulin plus CNZ on oxidative stress parameters in the liver of diabetic male rats induced with streptozotocin (STZ) and subjected to forced swimming test (FST). MATERIALS AND METHODS: Diabetes was induced by a single intraperitoneal (i.p.) dose of STZ 60 mg/kg in male Wistar rats. Insulin (4 IU/kg) plus CNZ acute i.p. treatment (0.25 mg/kg) was administered 24, 5 and 1 h before the FST. Nondiabetic control rats received i.p. injections of saline (1 mL/kg). Protein oxidative damage was evaluated by carbonyl formation and the antioxidant redox parameters were analyzed by the measurements of enzymatic activities of the superoxide dismutase (SOD), catalase and glyoxalase I (GLO). Glycemia levels also were determined. RESULTS: Our present study has shown an increase in carbonyl content from diabetic rats subjected to FST (2.04 ± 0.55), while the activity of catalase (51.83 ± 19.02) and SOD (2.30 ± 1.23) were significantly decreased in liver from these animals, which were reverted by the treatment. Also, the activity of GLO (0.15 ± 0.02) in the liver of the animals was decreased. DISCUSSION AND CONCLUSION: Our findings showed that insulin plus CNZ acute treatment ameliorate the antioxidant redox parameters and protect against protein oxidative damage in the liver of diabetic rats subjected to FST.