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首页> 外文期刊>Journal of Neurophysiology >Synaptic and network consequences of monosynaptic nociceptive inputs of parabrachial nucleus origin in the central amygdala
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Synaptic and network consequences of monosynaptic nociceptive inputs of parabrachial nucleus origin in the central amygdala

机译:中央杏仁核的臂旁旁核单突触伤害性输入的突触和网络后果

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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.
机译:背角浅层中的大部分神经元突出到臂外侧臂旁核(LPB)。然后,LPB神经元投射到中央杏仁核(CeA; CeC)的荚膜部分,这是伤害感受-情感联系背后的关键结构。通过使用电刺激脑切片中LPB起源的推定纤维,在各种疼痛模型中LPB-CeC突触传递得到增强。但是,这种方法在检查直接单突触连接方面缺乏局限性,而这种连接没有直接刺激来自其他结构和局部GABA能神经元的纤维。为了克服这些限制,我们用表达channelrhodopsin-2的腺相关病毒载体感染了大鼠的LPB,并制备了包含杏仁核的冠状和水平脑切片。我们发现,蓝光刺激会导致单突触兴奋性突触后电流(EPSC),潜伏期波动很小,然后在CeC神经元中会产生大的多突触抑制性突触后电流,而与放电模式类型无关。切片制备前24 h进行足底福尔马林注射,可明显增加晚期放电型CeC神经元的EPSC振幅。这些结果表明,来自LPB的直接单突触谷氨酸能输入不仅可以激发CeC神经元,而且还可以通过强大的前馈抑制作用来调节CeA网络信号,该作用在持续性炎性疼痛的响应下受到塑性调节。

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