Myelin-oligodendroglia complex in rats subjected to experimental cardiac arrest

Pathophysiology of oligodendroglial excitotoxicity

“…Since cells of the oligodendroglial lineage express non-NMDA-GluR, though not NMDA-GluR Patneau et al, 1994;Gallo and Russell, 1995;Liu and Almazan, 1995;Yoshioka et al, 1995;Mennerick et al, 1996;Meucci et al, 1996) we wondered whether the loss of oligodendroglia from ischemic or inflammatory lesions (Lifer et al, 1990;Prineas et al, 1993;Raine and Wu, 1993;Wender and Szczech, 1994) could be a consequence of excitotoxicity. In a previous article, we showed that cells of the oligodendroglial lineage are vulnerable to excitotoxicity; LDH release assays demonstrated diminished integrity of the plasma membranes of OLC exposed in cell culture to kainate, or to AMPA in the presence of the desensitization blocker, cyclothiazide.…”

“…This injury was prevented by the non-NMDAGluR blocker, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), but not by the L-glutamate transporter blocker, D,L-threo-P-hydroxyaspartate (Yoshioka et al, 1995). These data indicated that OLC are vulnerable to Ca2+ dependent, non-NMDA-GluR-mediated excitotoxicity , and suggested that excitotoxicity could be responsible for oligodendroglial depletion in foci of central nervous system (CNS) ischemia or inflammation (Leifer et al, 1990;Giulian et al, 1993;Prineas et al, 1993;Raine and Wu, 1993;Wender and Szczech, 1994), in which regulation of extracellular concentrations of excitatory amino acids is perturbed.…”

Cyclic GMP/Cyclic GMP‐Dependent Protein Kinase System Prevents Excitotoxicity in an Immortalized Oligodendroglial Cell Line

“…Excitotoxicity has been implicated in oligodendroglial depletion from foci of CNS ischemia or inflammation (Leifer et al., 1990; Giulian et al, 1993; Prineas et al, 1993; Raine and Wu, 1993; Wender and Szczech, 1994). In a recent study, we showed that oxygen‐glucose deprivation‐induced oligodendroglial damage was prevented by non‐NMDA GluR antagonists or by deprivation of extracellular Ca 2+ , but not by nimodipine, thus indicating that Ca 2+ influx through non‐NMDA GluR channels mediates oxygen‐glucose deprivation‐induced oligodendroglial death (Yoshioka et al, unpublished observations).…”