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1.
J Neural Transm (Vienna) ; 122(5): 709-19, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25182413

RESUMO

Exposure to stressful events early in life may have permanent deleterious consequences on nervous system function and increase the susceptibility to psychiatric conditions later in life. Maternal deprivation, commonly used as a source of neonatal stress, impairs memory in adult rats and reduces hippocampal brain-derived neurotrophic factor (BDNF) levels. Inflammatory cytokines, such as interleukins (IL) and tumor necrosis factor-α (TNF-α) have been shown to be increased in the peripheral blood of patients with psychiatric disorders. The aim of the present study was to investigate the effects of maternal separation on the levels of IL-10 and TNF-α, and BDNF in the hippocampus and prefrontal cortex of adult rats. We also evaluated the potential ameliorating properties of topiramate and valproic acid on memory deficits and cytokine and BDNF changes associated with maternal deprivation. The results indicated that, in addition to inducing memory deficits, maternal deprivation increased the levels of IL-10 in the hippocampus, and TNF-α in the hippocampus and in the cortex, and decreased hippocampal levels of BDNF, in adult life. Neither valproic acid nor topiramate were able to ameliorate memory deficits or the reduction in BDNF induced by maternal separation. The highest dose of topiramate was able to reduce IL-10 in the hippocampus and TNF-α in the prefrontal cortex, while valproate only reduced IL-10 levels in the hippocampus. These findings may have implications for a better understanding of the mechanisms associated with alterations observed in adult life induced by early stressful events, and for the proposal of novel therapeutic strategies.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Citocinas/metabolismo , Hipocampo/metabolismo , Privação Materna , Transtornos da Memória/metabolismo , Córtex Pré-Frontal/metabolismo , Animais , Comportamento Exploratório/efeitos dos fármacos , Comportamento Exploratório/fisiologia , Frutose/análogos & derivados , Frutose/farmacologia , Hipocampo/efeitos dos fármacos , Hipocampo/crescimento & desenvolvimento , Masculino , Transtornos da Memória/tratamento farmacológico , Transtornos da Memória/etiologia , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/crescimento & desenvolvimento , Psicotrópicos/farmacologia , Ratos Wistar , Reconhecimento Psicológico/efeitos dos fármacos , Reconhecimento Psicológico/fisiologia , Estresse Psicológico/tratamento farmacológico , Estresse Psicológico/etiologia , Estresse Psicológico/metabolismo , Topiramato , Ácido Valproico/farmacologia
2.
Mol Neurobiol ; 49(1): 222-33, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23893294

RESUMO

We have recently shown that chronic treatment with cannabidiol (CBD) was able to recover memory deficits induced by brain iron loading in a dose-dependent manner in rats. Brain iron accumulation is implicated in the pathogenesis of neurodegenerative diseases, including Parkinson's and Alzheimer's, and has been related to cognitive deficits in animals and human subjects. Deficits in synaptic energy supply have been linked to neurodegenerative diseases, evidencing the key role played by mitochondria in maintaining viable neural cells and functional circuits. It has also been shown that brains of patients suffering from neurodegenerative diseases have increased expression of apoptosisrelated proteins and specific DNA fragmentation. Here, we have analyzed the expression level of brain proteins involved with mitochondrial fusion and fission mechanisms (DNM1L and OPA1), the main integral transmembrane protein of synaptic vesicles (synaptophysin), and caspase 3, an apoptosis-related protein, to gain a better understanding of the potential of CBD in restoring the damage caused by iron loading in rats. We found that CBD rescued iron-induced effects, bringing hippocampal DNM1L, caspase 3, and synaptophysin levels back to values comparable to the control group. Our results suggest that iron affects mitochondrial dynamics, possibly trigging synaptic loss and apoptotic cell death and indicate that CBD should be considered as a potential molecule with memory-rescuing and neuroprotective properties to be used in the treatment of cognitive deficits observed in neurodegenerative disorders.


Assuntos
Canabidiol/farmacologia , Caspase 3/biossíntese , Dinaminas/biossíntese , Regulação da Expressão Gênica/efeitos dos fármacos , Sobrecarga de Ferro/metabolismo , Dinâmica Mitocondrial/fisiologia , Fármacos Neuroprotetores/farmacologia , Sinaptofisina/biossíntese , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Canabidiol/uso terapêutico , Feminino , Sobrecarga de Ferro/prevenção & controle , Masculino , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Dinâmica Mitocondrial/efeitos dos fármacos , Gravidez , Distribuição Aleatória , Ratos , Ratos Wistar
3.
Artigo em Português | LILACS | ID: biblio-882785

RESUMO

O tromboembolismo pulmonar é uma doença potencialmente grave, de difícil diagnóstico devido a apresentações diversas, exigindo diagnóstico rápido e a implementação de tratamento adequado. Torna-se importante a discussão sobre as novas alternativas no manejo medicamentoso contemporâneo desta patologia.


Pulmonary thromboembolism is a potentially serious disease, difficult to diagnose due to various presentations, requiring rapid diagnosis and implementation of appropriate treatment. It is important to discuss about new alternatives in contemporary medical management of this condition.


Assuntos
Anticoagulantes , Embolia Pulmonar/diagnóstico , Embolia Pulmonar/tratamento farmacológico
4.
Artigo em Português | LILACS | ID: biblio-882861

RESUMO

A Síndrome da Veia Cava Superior (SVCS) trata-se de uma manifestação clínica resultante da obstrução do fluxo sanguíneo ao nível da veia cava superior, podendo se manifestar em pacientes sem diagnóstico de base conhecido. O objetivo deste trabalho é revisar o manejo diagnóstico e terapêutico desses pacientes em atendimento de emergência.


Superior Vena Cava Syndrome is a clinical manifestation resulting from the obstruction of blood flow at the level of the Superior Vena Cava, which could manifest in patients without an etiologic diagnosis known. The objective of this work is to review the diagnosis and therapeutic management of these patients in emergency rooms.


Assuntos
Síndrome da Veia Cava Superior , Serviços Médicos de Emergência
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