Abstract
The amygdala plays significant roles in regulating emotional states and behaviors. Certain aspects of emotion are well known to be affected by the domaminergic projection system, of which targets includes the amygdala. Indeed, a large number of in vivo studies have shown that activation of dopamine (DA) receptors in lateral amygdala (LA) neurons alter emotional expression. For understanding DA-based modulation of emotion in the LA, it would therefore be beneficial to study effects of dopamine on intrinsic properties of the LA neurons, which remain largely unknown. In the present experiments, whole cell patch clamp recordings were carried out in rat brain slices to investigate DA effects on LA neurons. Application of DA depolarized resting membrane potential markedly, and induced slow afterdepolarization (sADP) in LA neurons. This sADP is induced in a voltage-dependent manner, and lasts for more than 5 seconds. D1, but not D2, receptor agonists induced the same type of sADP. Previous reports have repeatedly suggested that sADP in general is triggered by the calcium influx. Consistently, calcium channel blockers inhibited the present DA-induced sADP, but sodium channel blockers did not. Also, application of flufenamic acid (FFA), a calcium activated non-selective cation channel (CAN) blocker, inhibited the DA-induced sADP and canceled out the DA-induced depolarization as well. These results suggest that DA induces sADP in LA neurons by activating D1 receptors, and this sADP is attributable to activation of CANs. [J Physiol Sci. 2006;56 Suppl:S158]
