| First Author | Seiriki K | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 480 |
| Issue | 4 | Pages | 558-563 |
| PubMed ID | 27793672 | Mgi Jnum | J:240896 |
| Mgi Id | MGI:5896701 | Doi | 10.1016/j.bbrc.2016.10.089 |
| Citation | Seiriki K, et al. (2016) Critical involvement of the orbitofrontal cortex in hyperlocomotion induced by NMDA receptor blockade in mice. Biochem Biophys Res Commun 480(4):558-563 |
| abstractText | Glutamatergic N-methyl-d-aspartate (NMDA) receptors play critical roles in several neurological and psychiatric diseases. Blockade by noncompetitive NMDA receptor antagonist leads to psychotomimetic effects; however, the brain regions responsible for the effects are not well understood. Here, we determined the specific brain regions responsive to MK-801, a noncompetitive NMDA receptor antagonist, by mapping Arc expression as an indicator of neuronal activity using Arc::dVenus reporter mice. MK-801 increased dVenus expression predominantly in the orbitofrontal cortex (OFC) and, as expected, induced a marked hyperlocomotion. Local OFC lesions selectively attenuated the early phase (0-30 min) of MK-801-induced hyperlocomotion. Further, clozapine, an atypical antipsychotic, effectively attenuated both the MK-801-induced dVenus expression in the OFC and hyperlocomotion. These results suggest that the OFC may be critically involved in NMDA receptor-mediated psychotic-like behavioral abnormalities. |
