Target-specific suppression of GABA release from parvalbumin interneurons in the basolateral amygdala by dopamine.

Target-specific suppression of GABA release from parvalbumin interneurons in the basolateral amygdala by dopamine.
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DOI:
10.1523/jneurosci.2997-12.2012
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发表时间:
2012-10-17
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Morozov A
Morozov A
中科院分区:
其他
文献类型:
--
作者:
Chu HY;Ito W;Li J;Morozov A

文献摘要

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基底外侧杏仁核(BLA)中的多巴胺(DA)通过解除对主神经元(PN)的抑制并使其感觉输入中的突触可塑性成为可能来促进恐惧学习。虽然BLA中间神经元是异质的,但尚不清楚哪些中间神经元亚型在DA存在下减少对PN的GABA能输入。在这里,使用来自小鼠大脑的BLA切片中的通道视紫红质2的细胞类型选择性光刺激,我们研究了小清蛋白阳性中间神经元(PV-IN)的作用,PV-IN是BLA中的主要中间神经元亚群,我们发现DA通过作用于突触前D_2受体选择性地抑制GABA能从PV-IN向PN的传递,这种作用可被cAMP依赖性信号抑制剂Rp-cAMP模拟。相反,DA没有改变GABA从PV-INs释放到INs. Further,既不抑制cAMP依赖性信号的RP-cAMP,也不增强它由毛喉素改变GABA从PV-INs释放到BLA INs. Overall,DA disinhibit,至少部分,通过抑制GABA从PV-INs释放在靶细胞特异性的方式,这是由cAMP依赖性信号的差异控制这种释放的结果。
Dopamine (DA) in the basolateral amygdala (BLA) promotes fear learning by disinhibiting principal neurons (PNs) and enabling synaptic plasticity in their sensory inputs. While BLA interneurons are heterogeneous, it is unclear which interneuron subtypes decrease GABAergic input to PNs in the presence of DA. Here, using cell-type-selective photo-stimulation by channelrhodopsin 2 in BLA slices from mouse brain, we examined the role of parvalbumin-positive interneurons (PV-INs), the major interneuronal subpopulation in BLA, in the disinhibitory effect of DA. We found that DA selectively suppressed GABAergic transmission from PV-INs to PNs by acting on presynaptic D2 receptors and this effect was mimicked by Rp-cAMP, an inhibitor of cAMP-dependent signaling. In contrast, DA did not alter GABA release from PV-INs to INs. Furthermore, neither suppressing cAMP-dependent signaling by Rp-cAMP nor enhancing it by forskolin altered GABA release from PV-INs to BLA INs. Overall, DA disinhibits BLA, at least in part, by suppressing GABA release from PV-INs in the target-cell-specific manner which results from differential control of this release by cAMP-dependent signaling.