| First Author | Niimi K | Year | 2014 |
| Journal | Behav Brain Res | Volume | 259 |
| Pages | 45-9 | PubMed ID | 24177210 |
| Mgi Jnum | J:208303 | Mgi Id | MGI:5562623 |
| Doi | 10.1016/j.bbr.2013.10.033 | Citation | Niimi K, et al. (2014) Blockade of Cav2.1-mediated NMDA receptor signaling disrupts conditioned fear extinction. Behav Brain Res 259:45-9 |
| abstractText | Although fear extinction requires N-methyl-d-aspartate (NMDA) receptor signaling, Cav2.1-regulated synaptic function in extinction remains unknown. This study examined whether Cav2.1-mediated signaling plays role in consolidation of extinction. Wild-type mice received intracerebroventricular injection of Cav2.1 blocker (omega-agatoxin IVA, 4.0 pg/side) showed impaired extinction behavior and increased expression of CREB-dependent gene Arc in medial prefrontal cortex (mPFC). Intra-mPFC injections of NMDA receptor antagonist (MK-801, 0.5 mug/midline), which was ineffective in wild-type controls, blocked extinction in heterozygous rolling Nagoya (rol/+) mice carrying Cav2.1alpha1 gene mutation rol/+ mice. These results indicate that Cav2.1-mediated NMDA receptor signaling is functional pathway in mPFC-dependent fear extinction. Our results also indicate that the combination of pharmacological and genetic approaches can be used to study functional signaling pathways in neuronal circuits. |
