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多巴胺能调节大鼠基底外侧杏仁核的振荡网络抑制作用,取决于初始活动状态。

Dopaminergic modulation of oscillatory network inhibition in the rat basolateral amygdala depends on initial activity state.

机构信息

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.

出版信息

Neuropharmacology. 2011 Sep;61(4):857-66. doi: 10.1016/j.neuropharm.2011.06.002. Epub 2011 Jun 13.

DOI:10.1016/j.neuropharm.2011.06.002
PMID:21683087
Abstract

The amygdala receives dopaminergic innervation, and dopamine (DA) enhances various activities in cognitive and emotional behaviors. Periodic bursts of spontaneous inhibitory postsynaptic currents (IPSCs) with a low (<1 Hz) inter-event frequency have been observed in projection neurons of the basolateral nucleus of the amygdala (BL). Blockade of ionotropic glutamate receptors or GABA(A) receptors abolishes these oscillatory IPSC bursts in the BL, suggesting that the activity has a network origin. Here, we investigated dopaminergic modulation of the oscillatory network inhibition in rat brain slices. We evaluated the effects of DA receptor agonists and antagonists on the network inhibition; the resultant changes were quantified by integrated power spectral density (0.1-3.0 Hz). DA enhanced the power when its initial activity was low, but reduced it when the activity was initially robust. These changes in the power were accompanied by changes in burst IPSC amplitude. D1-like receptor agonist SKF 38393, or DA together with the D2-like receptor antagonist sulpiride, reproduced DA's facilitatory actions. D2-like receptor agonist quinpirole did not change the periodic IPSC burst activity of the high baseline power, though D(4) receptor agonist PD 168077, or DA together with the D1-like receptor antagonist SCH 23390, reduced its activity. These results suggest that: 1) dopaminergic modulation of the oscillatory network inhibition depends on its initial activity; and 2) facilitatory and suppressing effects of DA in the BL are mediated by D1-like receptors and D(4) receptors, respectively.

摘要

杏仁核接收多巴胺能神经支配,多巴胺 (DA) 增强认知和情绪行为的各种活动。在杏仁基底外侧核 (BL) 的投射神经元中观察到自发抑制性突触后电流 (IPSCs) 的周期性爆发,其事件间频率较低(<1 Hz)。离子型谷氨酸受体或 GABA(A) 受体的阻断消除了 BL 中的这些振荡 IPSC 爆发,表明该活动具有网络起源。在这里,我们研究了多巴胺能对大鼠脑片振荡网络抑制的调制。我们评估了 DA 受体激动剂和拮抗剂对网络抑制的影响;通过整合功率谱密度(0.1-3.0 Hz)对所得变化进行量化。当初始活动较低时,DA 增强了功率,但当活动最初较强时,它降低了功率。这些功率变化伴随着爆发 IPSC 幅度的变化。D1 样受体激动剂 SKF 38393,或 DA 与 D2 样受体拮抗剂舒必利一起,重现了 DA 的促进作用。D2 样受体激动剂喹吡罗不改变高基线功率的周期性 IPSC 爆发活动,尽管 D4 受体激动剂 PD 168077,或 DA 与 D1 样受体拮抗剂 SCH 23390,降低了其活性。这些结果表明:1) 振荡网络抑制的多巴胺能调制取决于其初始活动;2) BL 中 DA 的促进和抑制作用分别由 D1 样受体和 D4 受体介导。

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