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Magnetic Resonance Spectroscopy Studies on Changes in Cerebral Calcium and Zinc and the Energy State Caused by Excitotoxic Amino Acids
Author(s) -
Thatcher N. M.,
Prior M. J. W.,
Morris P. G.,
Bachelard H. S.
Publication year - 1999
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.1471-4159.1999.0722471.x
Subject(s) - excitotoxicity , glutamate receptor , nmda receptor , phosphocreatine , chemistry , calcium , hippocampal formation , biophysics , hippocampus , zinc , medicine , cortex (anatomy) , endocrinology , biochemistry , biology , receptor , neuroscience , energy metabolism , organic chemistry
Under control conditions, superfused hippocampal slicesexhibited a significantly higher phosphocreatine (PCr)/ATP ratio than corticalslices; the evidence suggests that this is due to lower concentrations of ATP,rather than higher concentrations of PCr. Glutamate caused relatively rapiddecreases in PCr and ATP levels to ∼45%, accompanied or immediatelyfollowed by an increased free intracellular calcium concentration([Ca 2+ ] i ) and the release of Zn 2+ in thecortex. In the hippocampus PCr and ATP decreased further to ∼20% ofcontrol values, but the changes in [Ca 2+ ] i andZn 2+ content were slower. This is in contrast to the effects ofdepolarisation, which produced the same rapid changes in the energy state and[Ca 2+ ] i , with no detectable Zn 2+ , in bothtissues. NMDA causes effects similar to those of glutamate in the cortex(decreases in the energy state, increased [Ca 2+ ] i , andrelease of Zn 2+ ). Pretreatment of the cortex for 1 h with the NMDAblocker MK‐801 prevented all of the observed effects of NMDA. In contrast,pretreatment with MK‐801 had no detectable effect on the increase in[Ca 2+ ] i or the decreases in PCr and ATP caused by glutamate, although it prevented the release of zinc. The results are discussed in relation to the function of the NMDA subtype of glutamate receptor in excitotoxicity.