RESUMO
INTRODUCTION: Lesion of the fimbria-fornix causes dysfunction of learning processes and has been used in animal models for the study of Alzheimer's disease. MATERIAL AND METHODS: With the objective of comparing the efficacy of two methods of producing a lesion of the fimbria-fornix, 40 young male Sprague-Dawley rats were distributed in four experimental groups: control (6), falsely lesioned (8), lesion due to aspiration (12) and lesion due to transection (14). RESULTS: The results showed that whilst with both techniques, in rats, serious cognitive defects were produced, as expressed by the high latencies of escape and small number of crossings of Morris's aquatic labyrinth, the aspiration lesion led to greater mortality than the transection lesion did. Similarly, the aspiration technique in rats induced hyperactivity, aggressiveness and tigmotaxia, while in the rats with lesions due to transection tigmotaxia ceased after their first attempts and hyperactivity on the second day of training. CONCLUSION: These results would suggest that a bilateral lesion due to transection of the fimbria-fornix is an effective alternative to an aspiration lesion to interrupt this pathway.
Assuntos
Fórnice/patologia , Fórnice/cirurgia , Doença de Alzheimer , Animais , Biópsia por Agulha/métodos , Transtornos Cognitivos/diagnóstico , Modelos Animais de Doenças , Aprendizagem/fisiologia , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
Introducción. La lesión de la fimbria-fornix causa disfunciones que afectan los procesos de aprendizaje y ha sido utilizada como modelo animal de enfermedad de Alzheimer. Material y métodos. Con el propósito de comparar la eficacia de dos métodos para producir la lesión de fimbria-fornix, se utilizaron 40 ratas machos jóvenes de la variedad Sprague-Dawley, distribuidas en cuatro grupos experimentales: controles (6), falsas lesionadas (8), lesionadas por aspiración (12), lesionadas por transección (14). Resultados. Los resultados mostraron que si bien ambas técnicas de lesión provocan en las ratas defectos cognitivos graves, según se expresa en las altas la
Assuntos
Modelos Animais de Doenças , Demência , Hipocampo , Memória , Fibras ColinérgicasRESUMO
Neurotrophins, like the nerve growth factor (NGF), trigger a variety of biological effects in their targets. Stimulating effects on antioxidant defenses have been postulated to underlie neurotrophic influence on neuron survival and maintenance. To test whether NGF is capable of inducing changes in glutathione-related enzymes in the aged cognitively impaired brain, glutathione reductase (GRD), glutathione S-transferase (GST) and total glutathione peroxidase (GPX) activities were measured in the striatum, septum, hippocampus and frontal cortex of four Sprague-Dawley rat groups: young (2 months old), aged (20 months old) untreated, aged cytochrome c-treated, and aged NGF-treated (icv delivery, 34 micrograms during 28 days). All the aged rats utilized in the study were memory impaired according to their performance in the Morris water maze test. These aged rats showed increases in the activities of septal and hippocampal GST, as well as, in the hippocampal, striatal and cortical GPX. These increases could be interpreted as compensatory responses to cope with the oxidative damage that has been accumulated by the aged brain. The increases in hippocampal and cortical GPX activity were attenuated by NGF treatment, whereas the neurotrophin induced an increase in GRD activity in the striatum of aged rats. These results point out GRD and GPX as possible targets of the neurotrophic effects.
Assuntos
Córtex Cerebral/efeitos dos fármacos , Glutationa Peroxidase/metabolismo , Glutationa Redutase/metabolismo , Glutationa Transferase/metabolismo , Hipocampo/efeitos dos fármacos , Fatores de Crescimento Neural/farmacologia , Análise de Variância , Animais , Córtex Cerebral/enzimologia , Transtornos Cognitivos/enzimologia , Transtornos Cognitivos/metabolismo , Ativação Enzimática , Hipocampo/enzimologia , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
Neurotrophins, like the nerve growth factor (NGF), trigger a variety of biological effects in their targets. Stimulating effects on antioxidant defenses have been postulated to underlie neurotrophic influence on neuron survival and maintenance. To test whether NGF is capable of inducing changes in glutathione-related enzymes in the aged cognitively impaired brain, glutathione reductase (GRD), glutathione S-transferase (GST) and total glutathione peroxidase (GPX) activities were measured in the striatum, septum, hippocampus and fraontal cortex of four Sprague-Dawley rat groups: young (2 months old), aged (20 months old) untreated, aged cytochrome c-treated, and aged NGF-treated (icv delivery, 34 æg during 28 days). All the aged rats utilized in the study were memory impaired according to their performance in the Morris water maze test. These aged rats showed increases in the activities of septal and hippocampal GST, as well as, in the hippocampal, striatal and cortical GPX. These increases could be interpreted as compensatory responses to cope with the oxidative damage that has been accumulated by the aged brain. The increases in hippocampal and corical GPX activity were attenuated by NGF treatment, whereas the neurotrophin induced an increase in GRD activity in the striatum of aged rats. These resultas point out GRD and GPX as possible targets of the neurotrophic effects
Assuntos
Humanos , Glutationa , Fatores de Crescimento Neural , EnvelhecimentoRESUMO
Neurotrophins, like the nerve growth factor (NGF), trigger a variety of biological effects in their targets. Stimulating effects on antioxidant defenses have been postulated to underlie neurotrophic influence on neuron survival and maintenance. To test whether NGF is capable of inducing changes in glutathione-related enzymes in the aged cognitively impaired brain, glutathione reductase (GRD), glutathione S-transferase (GST) and total glutathione peroxidase (GPX) activities were measured in the striatum, septum, hippocampus and fraontal cortex of four Sprague-Dawley rat groups: young (2 months old), aged (20 months old) untreated, aged cytochrome c-treated, and aged NGF-treated (icv delivery, 34 æg during 28 days). All the aged rats utilized in the study were memory impaired according to their performance in the Morris water maze test. These aged rats showed increases in the activities of septal and hippocampal GST, as well as, in the hippocampal, striatal and cortical GPX. These increases could be interpreted as compensatory responses to cope with the oxidative damage that has been accumulated by the aged brain. The increases in hippocampal and corical GPX activity were attenuated by NGF treatment, whereas the neurotrophin induced an increase in GRD activity in the striatum of aged rats. These resultas point out GRD and GPX as possible targets of the neurotrophic effects