Synaptic and network consequences of monosynaptic nociceptive inputs of parabrachial nucleus origin in the central amygdala.
Synaptic and network consequences of monosynaptic nociceptive inputs of parabrachial nucleus origin in the central amygdala.
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DOI：
10.1152/jn.00946.2015
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发表时间：
2016-06-01
影响因子：
2.5
通讯作者：
Kato F
中科院分区：
文献类型：
--
作者：
Sugimura YK;Takahashi Y;Watabe AM;Kato F
背角浅层的神经元大多投射到臂旁外侧核（LPB）。LPB神经元然后投射到中央杏仁核（CeA; CeC）的囊状部分，这是伤害感受-情绪联系的关键结构。在各种疼痛模型中，通过使用脑切片中LPB起源的推定纤维的电刺激来增强LPB-CeC突触传递。然而，这种方法在检查缺乏来自其他结构和局部GABA能神经元的直接刺激纤维的直接单突触连接时具有局限性。为了克服这些局限性，我们用表达通道视紫红质-2的腺相关病毒载体感染大鼠的LPB，并制备含有杏仁核的冠状和水平脑切片。我们发现，蓝光刺激导致单突触兴奋性突触后电流（EPSC），具有非常小的潜伏期波动，其次是一个大的多突触抑制性突触后电流在CeC神经元，无论发射模式类型。在切片制备前24 h足底注射福尔马林可显著增加晚放电型CeC神经元EPSC的振幅。这些结果表明，从LPB的直接单突触神经元的输入不仅兴奋CeC神经元，但也调节CeA网络信号通过强大的前馈抑制，这是下塑性调制响应于持续的炎症性疼痛。
A large majority of neurons in the superficial layer of the dorsal horn projects to the lateral parabrachial nucleus (LPB). LPB neurons then project to the capsular part of the central amygdala (CeA; CeC), a key structure underlying the nociception-emotion link. LPB-CeC synaptic transmission is enhanced in various pain models by using electrical stimulation of putative fibers of LPB origin in brain slices. However, this approach has limitations for examining direct monosynaptic connections devoid of directly stimulating fibers from other structures and local GABAergic neurons. To overcome these limitations, we infected the LPB of rats with an adeno-associated virus vector expressing channelrhodopsin-2 and prepared coronal and horizontal brain slices containing the amygdala. We found that blue light stimulation resulted in monosynaptic excitatory postsynaptic currents (EPSCs), with very small latency fluctuations, followed by a large polysynaptic inhibitory postsynaptic current in CeC neurons, regardless of the firing pattern type. Intraplantar formalin injection at 24 h before slice preparation significantly increased EPSC amplitude in late firing-type CeC neurons. These results indicate that direct monosynaptic glutamatergic inputs from the LPB not only excite CeC neurons but also regulate CeA network signaling through robust feed-forward inhibition, which is under plastic modulation in response to persistent inflammatory pain.