| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4180331 | Biological Psychiatry | 2007 | 10 Pages |
Abstract
Chronic CBZ administration to rats blocks increments in the AA signal k*, and in PGE2 and TXB2 concentrations that are produced by NMDA in vehicle-treated rats. The clinical action of antimanic drugs might involve inhibition of brain NMDAR-mediated signaling involving AA and its metabolites.
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Authors
Mireille Basselin, Nelly E. Villacreses, Mei Chen, Jane M. Bell, Stanley I. Rapoport,