Thus, there is a need to reassess what cerebral

localization of functions is and is not. Otherwise, there is no rational way to interpret the escalating claims of localization in the functional imaging literature that is taking on the appearance of neurophysiologic “”phrenology”". This article will present arguments to suggest that functional localization in the brain is a robust but very dynamic, four-dimensional process. It is a learned phenomenon driven over time by large-scale, spatially distributed, neural networks seeking to efficiently maximize the processing, storage, and manipulation of information for cognitive and behavioral operations. Because of historical considerations and space limitations, the main focus will be on localization of language-related https://www.selleckchem.com/products/SB-431542.html functions whose theoretical neurological basis can be generalized for any complex cognitive-behavioral

function.”
“Neurons respond to numerous factors in their environment that influence their survival and function during development and in the mature brain, Among these factors, the neurotrophins have been shown to support neuronal survival and function, acting primarily through the Trk family of receptor tyrosine kinases. However, recent studies have established that the uncleaved neurotrophin precursors, the proneurotrophins, can be secreted www.selleckchem.com/products/obeticholic-acid.html and induce apoptosis via the p75 neurotrophin receptor, suggesting that the balance of secreted mature and proneurotrophins has a critical impact on neuronal survival or death. Epileptic seizures elicit increases in both proneurotrophin secretion and p75(NTR) expression, shifting the balance of these factors toward signaling cell death. This review will discuss the evidence that this ligand-receptor system plays an important role in neuronal loss following seizures.”
“Epilepsy accounts for 0.5% of the global burden of disease, and primary prevention of epilepsy represents one of the three 2007 NINDS Epilepsy Research Benchmarks. In the past decade, efforts to understand and intervene in the process of epileptogenesis have yielded fruitful preventative strategies in animal models.

This article reviews the current understanding of epileptogenesis, introduces the concept of a “”critical period”" for epileptogenesis, and MEK162 in vitro examines strategies for epilepsy prevention in animal models of both acquired and genetic epilepsies. We discuss specific animal models,which may yield important insights into epilepsy prevention including kindling, poststatus epilepticus, prolonged febrile seizures, traumatic brain injury, hypoxia, the tuberous sclerosis mouse model, and the WAG/Rij rat model of primary generalized epilepsy. Hopefully, further investigation of antiepileptogenesis in animal models will soon enable human therapeutic trials to be initiated, leading to long-term epilepsy prevention and improved patient quality of life.