However, with certain NMDA antagonists, dose‐dependent vacuolization of neurons in the neuroanatomically localized PC/RS cortex occurs as a side effect in rats.
First-pass extracted concept
neuronal vacuolization in rat PC/RS cortex
Candidate: concept label1 source documents5 linked claims
Live refresh every 5sNext refresh in 5s
Evidence Snippets
Supporting Sources
Linked Claims
After MK-801 treatment, onset of vacuolization is very rapid.
Quoted textsource-backed
Electron microscopy has shown that after treatment with MK‐801 (dizocilpine maleate), a prototypic noncompetitive NMDA antagonist, the onset of vacuolization is very rapid.
As MK-801 dose increases, some vacuolated neurons become necrotic.
Quoted textsource-backed
Histologic time course studies have demonstrated that as the dose of MK‐801 is increased, some vacuolated neurons become necrotic.
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.
Susceptibility to MK-801-induced vacuolization increases between 30 and 90 days of age in rats.
Quoted textsource-backed
Additional studies with MK‐801 have indicated that susceptibility to vacuolization increases between 30 and 90 days of age.