| First Author | Tchekalarova J | Year | 2007 |
| Journal | Neurosci Lett | Volume | 415 |
| Issue | 1 | Pages | 68-72 |
| PubMed ID | 17289261 | Mgi Jnum | J:119743 |
| Mgi Id | MGI:3703209 | Doi | 10.1016/j.neulet.2006.12.040 |
| Citation | Tchekalarova J, et al. (2007) Angiotensin II suppresses long-term depression in the lateral amygdala of mice via L-type calcium channels. Neurosci Lett 415(1):68-72 |
| abstractText | Previously we have shown that angiotensin II (Ang II) suppresses long-term potentiation (LTP) in the lateral nucleus of the amygdala (LA) of horizontal slices. This study examines the effect of Ang II on long-term depression (LTD) in the LA. Low frequency stimulation (1Hz, 15min; LFS) applied to fibers running within the LA induced a long-lasting reduction of the amplitudes of field potentials in the LA of mice. We have previously shown that this LTD is sensitive to the NMDA receptor blocker D-AP5 and is dependent on group II mGlu receptors. Ang II blocked dose-dependent LTD. Losartan, an AT(1) receptor antagonist, blocked the Ang II-induced suppression of LTD, whereas PD 123 319, an AT(2) receptor antagonist, had no effect. Co-administration of nifedipine, an L-type calcium channel antagonist, abolished Ang II-induced suppression of LTD. When applied alone nifedipine reduced the magnitude of LA-LTD. According to our previous results, stimulation of external capsule (EC) fibers in rats did not cause LTD in mice. Similarly, Ang II did not induce long-lasting changes of activity when EC stimulation site was used. The results support the view that angiotensins are involved in mechanisms of learning and memory including the plasticity changes in the LA. |
