RESUMO

Life experiences at early ages, such as physical activity in childhood and adolescence, can result in long-lasting brain effects able to reduce future risk of brain disorders and to enhance lifelong brain functions. However, how early physical exercise promotes these effects remains unclear. A possible hypothesis is that physical exercise increases the expression of neurotrophic factors and stimulates neuronal growth, resulting in a neural reserve to be used at later ages. Basing our study on this hypothesis, we evaluated the absolute number and morphology of neuronal cells, as well as the expression of growth, proliferation and survival proteins (BDNF, Akt, mTOR, p70S6K, ERK and CREB) in the cerebral cortex and hippocampal formation throughout of a sedentary period of rats who were physically active during youth. To do this, male Wistar rats were submitted to an aerobic exercise protocol from the 21st to the 60th postnatal days (P21-P60), and evaluated at 0 (P60), 30 (P90) and 60 (P120) days after the last exercise session. Results showed that juvenile exercise increased, and maintained elevated, the number of cortical and hippocampal neuronal cells and dendritic arborization, when evaluated at the above post-exercise ages. Hippocampal BDNF levels and cortical mTOR expression were found to be increased at P60, but were restored to control levels at P90 and P120. Overall, these findings indicate that, despite the short-term effects on growth and survival proteins, early exercise induces long-lasting morphological changes in cortical and hippocampal neurons even during a sedentary period of rats.

Assuntos

Córtex Cerebral/citologia , Hipocampo/citologia , Plasticidade Neuronal/fisiologia , Neurônios/citologia , Condicionamento Físico Animal/fisiologia , Hormônio Adrenocorticotrópico/metabolismo , Animais , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Forma Celular/fisiologia , Córtex Cerebral/metabolismo , Córtex Cerebral/fisiologia , Corticosterona/metabolismo , Dendritos/fisiologia , Hipocampo/metabolismo , Hipocampo/fisiologia , Masculino , Neurônios/metabolismo , Neurônios/fisiologia , Ratos , Ratos Wistar , Serina-Treonina Quinases TOR/metabolismo

RESUMO

Traumatic brain injury (TBI) is a devastating condition which often initiates a sequel of neurological disorders that can last throughout lifespan. From metabolic perspective, TBI also compromises systemic physiology including the function of body organs with subsequent malfunctions in metabolism. The emerging panorama is that the effects of TBI on the periphery strike back on the brain and exacerbate the overall TBI pathogenesis. An increasing number of clinical reports are alarming to show that metabolic dysfunction is associated with incidence of long-term neurological and psychiatric disorders. The autonomic nervous system, associated hypothalamic-pituitary axis, and the immune system are at the center of the interface between brain and body and are central to the regulation of overall homeostasis and disease. We review the strong association between mechanisms that regulate cell metabolism and inflammation which has important clinical implications for the communication between body and brain. We also discuss the integrative actions of lifestyle interventions such as diet and exercise on promoting brain and body health and cognition after TBI.

Assuntos

Doenças do Sistema Nervoso Autônomo , Lesões Encefálicas Traumáticas , Inflamação , Síndrome Metabólica , Plasticidade Neuronal , Doenças do Sistema Nervoso Autônomo/etiologia , Doenças do Sistema Nervoso Autônomo/imunologia , Doenças do Sistema Nervoso Autônomo/metabolismo , Doenças do Sistema Nervoso Autônomo/fisiopatologia , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/imunologia , Lesões Encefálicas Traumáticas/metabolismo , Lesões Encefálicas Traumáticas/fisiopatologia , Humanos , Inflamação/etiologia , Inflamação/imunologia , Inflamação/metabolismo , Inflamação/fisiopatologia , Síndrome Metabólica/etiologia , Síndrome Metabólica/imunologia , Síndrome Metabólica/metabolismo , Síndrome Metabólica/fisiopatologia , Plasticidade Neuronal/fisiologia

RESUMO

Better cognitive performance and greater cortical and hippocampal volume have been observed in individuals who undertook aerobic exercise during childhood and adolescence. One possible explanation for these beneficial effects is that juvenile physical exercise enables better neural development and hence more cells and neuronal circuitries. It is probable that such effects occur through intracellular signaling proteins associated with cell growth, proliferation and survival. Based on this information, we evaluated the number of neuronal and non-neuronal cells using isotropic fractionation and the expression and activation of intracellular proteins (ERK, CREB, Akt, mTOR and p70S6K) in the cerebral cortex and hippocampal formation of the rats submitted to a physical exercise program on a treadmill during adolescence. Results showed that physical exercise increases the number of neuronal and non-neuronal cortical cells and hippocampal neuronal cells in adolescent rats. Moreover, mTOR overexpression was found in the cortical region of exercised adolescent rats. These findings indicate a significant cellular proliferative effect of aerobic exercise on the cerebral cortex in postnatal development.

Assuntos

Córtex Cerebral/metabolismo , Memória/fisiologia , Plasticidade Neuronal/fisiologia , Condicionamento Físico Animal/fisiologia , Serina-Treonina Quinases TOR/metabolismo , Envelhecimento , Animais , Hipocampo/metabolismo , Masculino , Neurônios/metabolismo , Ratos Wistar , Transdução de Sinais/fisiologia

RESUMO

A large amount of evidence has demonstrated the power of exercise to support cognitive function, the effects of which can last for considerable time. An emerging line of scientific evidence indicates that the effects of exercise are longer lasting than previously thought up to the point to affect future generations. The action of exercise on epigenetic regulation of gene expression seem central to building an "epigenetic memory" to influence long-term brain function and behavior. In this review article, we discuss new developments in the epigenetic field connecting exercise with changes in cognitive function, including DNA methylation, histone modifications and microRNAs (miRNAs). The understanding of how exercise promotes long-term cognitive effects is crucial for directing the power of exercise to reduce the burden of neurological and psychiatric disorders.

Assuntos

Encéfalo/fisiologia , Cognição/fisiologia , Epigênese Genética , Atividade Motora/fisiologia , Plasticidade Neuronal/fisiologia , Animais , Humanos

RESUMO

Metabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders.