Increase of ATP levels by glutamate antagonists is unrelated to neuroprotection

M. Riepe, A. Ludolph, M. Seelig, P. S. Spencer, A. C. Ludolph

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

Succinic dehydrogenase in mouse cortical explant cultures was inhibited by 3-nitropropionic acid (3-NPA). ATP concentrations declined upon application of 3-NPA. At 4 h, ATP levels of cultures treated with 3-NPA alone were no different from those in cultures treated additionally with MK-801 (20 /xM), 6-cyano-7-nitroquinoxa- line-2,3-dione (CNQX; 10 /uM) or a combination thereof. However, MK-801 and MK-801 plus CNQX mitigated morphological lesions caused by 3-NPA. CNQX alone did not influence the extent of morphological damage. In conclusion, MK-801, at concentrations which were neuro- protective against 3-NPA lesions in cortical explant cultures, did not modify 3-NPA dependent decreases in cellular ATP levels. These data indicate that the neuropro- tective effects of glutamate receptor antagonists in this model are probably receptor mediated and do not involve effects on cellular metabolism.

Original languageEnglish (US)
Pages (from-to)2130-2132
Number of pages3
JournalNeuroReport
Volume5
Issue number16
DOIs
StatePublished - Oct 1994

Keywords

  • 3-NPA
  • ATP
  • Excitoxicity
  • Glutamate
  • Glutamate antagonist
  • Neurodegeneration
  • SDH

ASJC Scopus subject areas

  • Neuroscience(all)

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