RESUMO
BACKGROUND: Nicotine (NIC), the major active component of tobacco, is critical in the maintenance of the smoking habit. The aims of the present study were to analyze the behavioural and neurochemical variations during NIC withdrawal syndrome in mice, and whether they are prevented with baclofen (BAC, GABA(B) receptor agonist). METHODS: Swiss-Webster albino mice received NIC (2.5 mg/kg, s.c.) 4 times daily, for 7 consecutive days. On day 8 (the day of the experiment), NIC-treated mice received the nicotine antagonist mecamylamine (MEC, 2 mg/kg, i.p.) 1h after the last dose of NIC. A second group of dependent mice received BAC (2mg/kg, i.p.) before MEC-precipitated abstinence. The somatic signs were measured for 30 min. Dopamine (DA), serotonin (5-hydroxytryptamine; 5-HT) and its metabolites concentrations were determined by HPLC in the striatum, cortex and hippocampus. RESULTS: The global score was greater in the abstinent group compared to the control group. Moreover, the global score time course showed a higher increase at 10 min compared to the global score at 5 min or 30 min after MEC-precipitated NIC withdrawal. In addition, the global score was attenuated by BAC. The DA and dihydroxyphenyl acetic acid (DOPAC) cortical levels decreased in the abstinent group, while BAC reestablished these levels 10 min after NIC withdrawal. Furthermore, DA and 5-HT striatal levels decreased during NIC withdrawal, and BAC reverted this decrease. CONCLUSION: In conclusion, the prevention of NIC withdrawal signs by BAC could be related to changes in dopaminergic and serotonergic activity.
Assuntos
Baclofeno/farmacologia , Mecamilamina/efeitos adversos , Nicotina/efeitos adversos , Agonistas Nicotínicos/efeitos adversos , Antagonistas Nicotínicos/efeitos adversos , Síndrome de Abstinência a Substâncias/tratamento farmacológico , Síndrome de Abstinência a Substâncias/prevenção & controle , Animais , Baclofeno/sangue , Baclofeno/uso terapêutico , Comportamento Animal/efeitos dos fármacos , Modelos Animais de Doenças , Avaliação Pré-Clínica de Medicamentos , Masculino , Mecamilamina/sangue , Camundongos , Atividade Motora/efeitos dos fármacos , Nicotina/sangue , Agonistas Nicotínicos/sangue , Antagonistas Nicotínicos/sangue , Abandono do Hábito de Fumar/métodos , Síndrome de Abstinência a Substâncias/metabolismo , Fatores de TempoRESUMO
AIM: The goal of this histometric study was to compare the healing process of dehiscence-type defects treated by enamel matrix derivative (EMD) or guided tissue regeneration (GTR) under the effect of nicotine in the dog model. MATERIALS AND METHODS: Eight mongrel dogs were used. Buccal osseous dehiscences were surgically created on the mesial roots of the mandibular third and fourth pre-molars. The defects were exposed to plaque accumulation for 3 months. After this period, the defects were randomly assigned to one of the treatments: open flap debridement (OFD), EMD or GTR with a resorbable membrane. During 4 months, the dogs received subcutaneous administration of nicotine (2 mg/kg twice a day with a 12 h interval between the applications). After this period, the animals were killed and the blocks were processed. The histometric parameters evaluated included gingival recession, epithelial length, connective tissue adaptation, new cementum and new bone. RESULTS: A superior length of new cementum was observed in the sites treated by EMD in comparison with OFD (p< or =0.05). No statistically significant differences were observed between GTR and the other groups. CONCLUSIONS: In the presence of nicotine, EMD may promote more new cementum formation than OFD while GTR failed to provide a significant difference.
Assuntos
Perda do Osso Alveolar/cirurgia , Materiais Biocompatíveis/uso terapêutico , Proteínas do Esmalte Dentário/uso terapêutico , Regeneração Tecidual Guiada Periodontal/métodos , Nicotina/administração & dosagem , Agonistas Nicotínicos/administração & dosagem , Implantes Absorvíveis , Perda do Osso Alveolar/patologia , Processo Alveolar/patologia , Animais , Tecido Conjuntivo/patologia , Cotinina/sangue , Desbridamento , Cemento Dentário/patologia , Placa Dentária/complicações , Modelos Animais de Doenças , Cães , Inserção Epitelial/patologia , Retração Gengival/patologia , Injeções Subcutâneas , Membranas Artificiais , Nicotina/sangue , Agonistas Nicotínicos/sangue , Distribuição Aleatória , Retalhos Cirúrgicos , Cicatrização/fisiologiaRESUMO
The concept of smoking has evolved considerably in recent decades. From a habit in the 1960s, tobacco consumption came to be viewed as a chemical dependency in the 1970s and an addiction in the 1980s, until smokers' clinics were implemented in the 1990s. To understand the mechanism of the smoking habit, it is important to recall that smoking represents much more than physical dependence on nicotine. Over time, smokers receive social, behavioral, and cultural stimuli that reinforce their habit and probably serve as the causal elements for establishing their psychological dependence. Both the psychological and physical components of tobacco dependence play a fundamental role in maintaining the habit.