Intracellular calcium ([Ca(2+)]i) influx through N-methyl-d-aspartic acid (NMDA) receptors in cortical neurons is central to NMDA receptor-mediated excitotoxicity. Drugs that uncompetitively modulate NMDA receptor-mediated [Ca(2+)]i influx are potential leads for development to treat NMDA receptor-mediated neuronal damage since these drugs spare NMDA receptor normal functions. Ligands to alpha(2)-adrenoceptors and imidazoline I(2) receptors confer neuroprotection possibility through modulating NMDA receptor-mediated [Ca(2+)]i influx.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2009
Basic fibroblast growth factor (bFGF) is a known neuroprotectant against a number of brain injury conditions such as cerebral ischemia. However, bFGF also regulates a plethora of brain developmental processes and functions as a strong mitogen. Therefore, unregulated long-term expression of bFGF in brain may potentially be tumorigenic, limiting its utility in brain therapy.
View Article and Find Full Text PDFThe pathophysiology of neurogenic inflammation culminates in the overt symptoms of tissue inflammation through a series of events which are initiated by the activation of vanilloid receptors (VR1). This study was designed to test the hypothesis that a sufficiently negative, electrostatic charge carried on a particulate matter (PM) particle, could acquire a cloud of protons sufficient to activate proton-sensitive VR1 receptors and acid-sensitive ionic channels (ASICs) pathways. For this, nanometer-sized, synthetic polystyrene micells (SPM) or those charged with chemical groups (e.
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