Pathological circumstances impair the ability of dark neurons to undergo spontaneous recovery
作者： Ferenc Gallyas , Balázs Gasz , András Szigeti , Mária Mázló
DOI: 10.1016/J.BRAINRES.2006.06.078
关键词: Biophysics 、 Amiloride 、 Enzyme inhibitor 、 Biochemistry 、 Pinacidil 、 Chemistry 、 Potassium channel 、 Veratridine 、 Neuron 、 Tetraethylammonium chloride 、 Sodium channel
摘要: The effects of dehydrating drugs (furosemide, mannitol and glycerine), potassium channel modulators (tetraethylammonium chloride, 5-hydroxydecanoic acid Na salt, minoxidil pinacidil), sodium (veratridine, brevetoxin-9, 5-(N,N-dimethyl)amiloride benzamil–HCl) mitochondrial enzyme inhibitors (3-nitropropionic acid, 2,4-dinitrophenol chloramphenicol) on the fate electrically produced “dark” hippocampal dentate granule neurons were investigated. All but one (chloramphenicol) these bioactive reagents substantially retarded recovery increased death rate such neurons. As concerns ion modulators, are considered to be consequences fact that relatively large volumes (more than half original cell volume) cytoplasmic fluid (water molecules, inorganic ions metabolites) leave affected cells through passive pores within a few minutes. appear indicate restoration volume (recovery) demands metabolic (enzyme-mediated) energy. features support our previous assumption exogenous circumstances existing acutely after formation in neurological diseases decide whether they will recover or die.
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