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DCG‐IV Selectively Attenuates Rapidly Triggered NMDA‐induced Neurotoxicity in Cortical Neurons

DCG‐IV Selectively Attenuates Rapidly Triggered NMDA‐induced Neurotoxicity in Cortical Neurons 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 μM NMDA. This neuroprotective effect was reversed by coapplication of α‐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, α‐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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

DCG‐IV Selectively Attenuates Rapidly Triggered NMDA‐induced Neurotoxicity in Cortical Neurons

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References (39)

Publisher
Wiley
Copyright
Copyright © 1996 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1111/j.1460-9568.1996.tb01174.x
Publisher site
See Article on Publisher Site

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 μM NMDA. This neuroprotective effect was reversed by coapplication of α‐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, α‐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.

Journal

European Journal of NeuroscienceWiley

Published: Jan 1, 1996

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