This review discusses available information on the neurotoxicity of N‐methyl‐D‐aspartate (NMDA) antagonists in the posterior cingulate/retrosplenial (PC/RS) cortex of rats.
First-pass extracted concept
NMDA antagonist-mediated PC/RS cortical neurotoxicity
Candidate: concept label1 source documents4 linked claims
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Linked Claims
Certain NMDA antagonists cause dose-dependent neuronal vacuolization in rat posterior cingulate/retrosplenial cortex.
Quoted textsource-backed
However, with certain NMDA antagonists, dose‐dependent vacuolization of neurons in the neuroanatomically localized PC/RS cortex occurs as a side effect in rats.
Compounds with anticholinergic, GABAmimetic, antipsychotic, and general anesthetic activity can partially or completely prevent neuronal vacuolization caused by NMDA antagonists.
Quoted textsource-backed
A number of compounds with varied central nervous system (CNS) pharmacologic activity (anticholinergics, GABAmimetics, antipsychotics, and general anesthetics) partially or completely prevent neuronal vacuolization.
NMDA antagonists that cause vacuolization also appear to induce heat shock protein expression and heightened glucose metabolism in the same cortical region.
Quoted textsource-backed
NMDA antagonists that cause vacuolization also appear to induce heat shock protein expression and heightened glucose metabolism in the same cortical region.
The neurotoxic side effects discussed in this review may not apply to all NMDA antagonists.
Quoted textsource-backed
Since recent reports have described failure of some NMDA antagonists to produce these side effects, the issues discussed in this review may or may not apply to all NMDA antagonists.