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      DCG-IV selectively attenuates rapidly triggered NMDA-induced neurotoxicity in cortical neurons.

      1 , ,
      The European journal of neuroscience

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          Abstract

          Molecular cloning has revealed the existence of at least eight subtypes of metabotropic glutamate receptors (mGluRs). We examined the effect of (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV), a selective agonist of the mGluR 2/3 subtype, on excitotoxicity in mouse cortical cell cultures. Addition of DCG-IV to the exposure medium partially attenuated the rapidly triggered excitotoxic death induced by a 5 min exposure to 200 microM NMDA. This neuroprotective effect was reversed by coapplication of alpha-methyl-4-carboxyphenylglycine (MCPG), an antagonist of mGluRs, by pertussis toxin pretreatment and also by preincubation with dibutyryl cAMP, a stable analogue of cAMP. These results suggest that the activation of mGluR 2/3 is neuroprotective in our system. However, DCG-IV did not attenuate the slowly triggered neuronal death induced by 24 h exposure to low concentrations of NMDA, alpha-amino-1,3-cyclopentanedicarboxylic acid (AMPA) or kainate. The failure of DCG-IV to block slowly triggered NMDA neurotoxicity is likely due to weak NMDA agonist activity, as demonstrated in whole-cell recording.

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          Author and article information

          Journal
          Eur. J. Neurosci.
          The European journal of neuroscience
          0953-816X
          0953-816X
          Jan 1996
          : 8
          : 1
          Affiliations
          [1 ] Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA.
          Article
          8713457
          49a8e869-0e9c-45e9-8a48-69a9450fe235
          History

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