1,721,127 research outputs found

    Different rates of horseradish peroxidase transport in the optic nerve of neonatal and adult rats

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    In order to evaluate the effects of age upon fast transport kinetics, we studied the velocity of horseradish peroxidase transport along the optic pathway of neonatal and adult rats. Rate of horseradish peroxidase movement was assessed by following the displacement of horseradish peroxidase activity in the optic nerve with time after injection. We estimated a rate of about 100 mm/day for bidirectional transport of horseradish peroxidase in the optic nerve of neonatal rats, while a two-fold higher rate was observed for anterograde transport in adult animals. Developmental regulation of fast transport rate may ensure relative constancy of the time required to connect the cell body with axon terminals

    Epilepsy: synapses stuck in childhood

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    Mouse experiments show how mutation of a gene involved in human epilepsy causes hyperexcitability of the neuronal network (pages 1208-1214). The mutations interfere with the maturation of excitatory synapses during postnatal development. © 2009 Nature America, Inc. All rights reserved

    Neurotrophins and plasticity in the visual cortex

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    The visual cortex is one of the favorite models for the study of experience-dependent changes in neuronal structure and function. A number of recent investigations indicate that the neurotrophic factors of the nerve growth factor family (neurotrophins) play a pivotal role in visual cortical plasticity. Neurotrophins and their receptors are present in the cortex during the critical period for plasticity, and neurotrophin levels are regulated by electrical activity. Neurotrophins modulate synaptic transmission and patterns of neuronal connectivity in the cortex. This review summarizes the in vivo and in vitro data that demonstrate the involvement of neurotrophins in visual cortical plasticity and discusses the possible mechanisms of their action

    Epilepsy, Seizures, and Inflammation: Role of the C-C Motif Ligand 2 Chemokine

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    Epilepsy is a chronic disorder characterized by spontaneous recurrent seizures. Several lines of evidence demonstrate that inflammatory processes within the brain parenchyma contribute to recurrence and precipitation of seizures. In both epileptic patients and animal models, seizures upregulate inflammatory mediators, which in turn may enhance brain excitability. We recently showed that the C-C motif ligand 2 (CCL2) chemokine (also known as monocyte chemoattractant protein-1 [MCP-1]) mediates the seizure-promoting effects of inflammation. Systemic inflammatory challenge in chronically epileptic mice markedly enhanced seizure frequency and upregulated CCL2 expression in the brain. Selective pharmacological blockade of CCL2 synthesis or C-C chemokine receptor type 2 (CCR2) significantly suppressed inflammation-induced seizures. These results have important implications for the development of novel anticonvulsant therapies: drugs interfering with CCL2 signaling are used clinically for several human disorders and might be redirected for use in pharmacoresistant epilepsy. Here we review the role of CCL2/CCR2 signaling in linking systemic inflammation with seizure susceptibility and discuss some open questions that arise from our recent studies
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