Excitotoxic Amino Acids Cause Appearance of Magnetic Resonance Spectroscopy‐Observable Zinc in Supervised Cortical Slices

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Abstract
(1) The effects of glutamate and NMDA on the free intracellular calcium concentration ([Ca2+],) have been followed in superfused cortical slices using the 19F‐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 [Ca2+], 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 [Ca2+], and was independent of Mg2+. (3) NMDA, N‐methyl‐dl‐aspartate, or N‐methyl‐l‐aspartate (10–200 μM) caused a slower increase in [Ca2+], and zinc was observed in some but not all experiments. When present, zinc appeared later than the increase in [Ca2+] These changes were also independent of Mg2+. (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 O2 (where increases also occur in [Da2+],), 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.

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