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- W2000213829 abstract "Both ionotropic and metabotropic glutamate receptors have been implicated in the pathogenesis of neuronal injury. Activation of group I metabotropic glutamate receptors (mGluR) exacerbates neuronal cell death, whereas inhibition is neuroprotective. However, the mechanisms involved remain unknown. Activation of group I mGluR modulates multiple signal transduction pathways including stimulation of phosphoinositide hydrolysis, potentiation of NMDA receptor activity, and release of arachidonic acid. Here we demonstrate that whereas activation of group I mGluR by (S)-3,5-dihydroxyphenylglycine (DHPG) potentiates NMDA-induced currents and intracellular calcium increases in rat cortical neuronal cultures, partial effects of group I mGluR activation or inhibition on neuronal injury induced by oxygen-glucose deprivation remain despite NMDA receptor blockade. DHPG stimulation also increases basal arachidonic acid release from rat neuronal-glial cultures and potentiates injury-induced arachidonic acid release in these cultures. Thus, activation of group I mGluR may exacerbate neuronal injury through multiple mechanisms, which include positive modulation of NMDA receptors and enhanced release of arachidonic acid." @default.
- W2000213829 created "2016-06-24" @default.
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- W2000213829 date "2001-06-01" @default.
- W2000213829 modified "2023-10-13" @default.
- W2000213829 title "Exacerbation of Neuronal Cell Death by Activation of Group I Metabotropic Glutamate Receptors: Role of NMDA Receptors and Arachidonic Acid Release" @default.
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- W2000213829 doi "https://doi.org/10.1006/exnr.2001.7672" @default.
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