Pathological circumstances impair the ability of "dark" neurons to undergo spontaneous recovery

Ferenc Gallyas, Balázs Gasz, András Szigeti, Mária Mázló

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The effects of dehydrating drugs (furosemide, mannitol and glycerine), potassium channel modulators (tetraethylammonium chloride, 5-hydroxydecanoic acid Na salt, minoxidil and pinacidil), sodium channel modulators (veratridine, brevetoxin-9, 5-(N,N-dimethyl)amiloride and benzamil-HCl) and mitochondrial enzyme inhibitors (3-nitropropionic acid, 2,4-dinitrophenol and chloramphenicol) on the fate of electrically produced "dark" hippocampal dentate granule neurons were investigated. All but one (chloramphenicol) of these bioactive reagents substantially retarded the recovery and increased the death rate of such "dark" neurons. As concerns the dehydrating drugs and ion channel modulators, these effects are considered to be consequences of the fact that relatively large volumes (more than half of the original cell volume) of cytoplasmic fluid (water molecules, inorganic ions and metabolites) leave the affected cells through passive pores within a few minutes. The effects of the mitochondrial enzyme inhibitors appear to indicate that restoration of the original cell volume (recovery) demands metabolic (enzyme-mediated) energy. All these features support our previous assumption that the exogenous circumstances existing acutely after the formation of "dark" neurons in neurological diseases decide whether they will recover or die.

Original languageEnglish
Pages (from-to)211-220
Number of pages10
JournalBrain research
Volume1110
Issue number1
DOIs
Publication statusPublished - Sep 19 2006

Keywords

  • Dehydration
  • Electric shock
  • Enzyme inhibition
  • Ion channel modulation
  • Irreversible neuronal damage
  • Reversible neuronal damage

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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