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Excitotoxic Amino Acids Cause Appearance of Magnetic Resonance Spectroscopy‐Observable Zinc in Supervised Cortical Slices
Author(s) -
BadarGoffer Ronnitte,
Morris Peter,
Thatcher Nicola,
Bachelard Herman
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62062488.x
Subject(s) - nmda receptor , zinc , excitotoxicity , glutamate receptor , chemistry , depolarization , phosphocreatine , glutamic acid , biophysics , biochemistry , medicine , amino acid , endocrinology , receptor , biology , organic chemistry , energy metabolism
(1) The effects of glutamate and NMDA on the free intracellular calcium concentration ([Ca 2+ ],) have been followed in superfused cortical slices using the 19 F‐magnetic resonance indicator 1,2‐bis(2‐amino‐5‐fluorophenoxy)ethane‐ N , N , N '. N '‐tetra‐acetic acid (5FBAPTA). (2) Glutamate (0.5 or 1 m/W) caused a 75–100% increase in [Ca 2+ ], and a new resonance was attributed to zinc‐5FBAPTA, which was confirmed from its disappearance in the presence of a high‐affinity chelator of heavy metals, N , N , N ', N '‐tetrakis(2‐pyridylmethyl)ethylenediamine. The appearance of zinc occurred with or just after the rise in [Ca 2+ ], and was independent of Mg 2+ . (3) NMDA, N ‐methyl‐ dl ‐aspartate, or N‐ methyl‐ l ‐aspartate (10–200 μ M ) caused a slower increase in [Ca 2+ ], and zinc was observed in some but not all experiments. When present, zinc appeared later than the increase in [Ca 2+ ] These changes were also independent of Mg 2+ . (4) Decreases in both phosphocreatine and ATP were observed in all of these studies. (5) The results are discussed in terms of the proposed role of zinc as a modulator of excitotoxicity. Observations of zinc after exposure to glutamate or more slowly to NMDA, but not after depolarisation or deprivation of glucose and O 2 (where increases also occur in [Da 2+ ],), suggest that the cellular damage caused by the latter insults (depolarisation and fuel deprivation as in ischaemia) involves mechanisms not solely attributable to release of excitotoxins.