A comparison of some metabolic effects of N-methylaspartate stereoisomers, glutamate and depolarization: a multinuclear MRS study.

Exposure of guinea pig brain slices to low concentrations (10 microM) of NMDA caused decreases in PCr and ATP within 30 min, with a slower decrease in NAA and increase in lactate, both detectable after 1 h. Exposure to NMDA for over 1 h or at higher concentrations caused further increases in lactate and decreases in NAA, with no further change in PCr or ATP. The L-isomer, NMLA, and the racemic mixture, NMDLA, caused similar changes in lactate and NAA, but both produced greater decreases in the energy state than NMDA, similar to those caused by prolonged exposure to glutamate.

Excitotoxic amino acids cause appearance of magnetic resonance spectroscopy-observable zinc in superfused cortical slices.

(1) The effects of glutamate and NMDA on the free intracellular calcium concentration ([Ca2+]i) 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'-tetraacetic acid (5FBAPTA). (2) Glutamate (0.5 or 1 mM) caused a 75-100% increase in [Ca2+]i, 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.

Neither moderate hypoxia nor mild hypoglycaemia alone causes any significant increase in cerebral [Ca2+]i: only a combination of the two insults has this effect. A 31P and 19F NMR study.

(1) The energy state and free intracellular calcium concentration ([Ca2+]i) of superfused cortical slices were measured in moderate hypoxia (approximately 65 microM O2), in mild hypoglycaemia (0.5 mM glucose), and in combinations of the two insults using 19F and 31P NMR spectroscopy. (2) Neither hypoxia nor hypoglycaemia alone caused any significant change in [Ca2+]i.