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Synaptic control of spinal GRPR+ neurons by local and long-range inhibitory inputs.


ABSTRACT: Spinal gastrin-releasing peptide receptor-expressing (GRPR+) neurons play an essential role in itch signal processing. However, the circuit mechanisms underlying the modulation of spinal GRPR+ neurons by direct local and long-range inhibitory inputs remain elusive. Using viral tracing and electrophysiological approaches, we dissected the neural circuits underlying the inhibitory control of spinal GRPR+ neurons. We found that spinal galanin+ GABAergic neurons form inhibitory synapses with GRPR+ neurons in the spinal cord and play an important role in gating the GRPR+ neuron-dependent itch signaling pathway. Spinal GRPR+ neurons also receive inhibitory inputs from local neurons expressing neuronal nitric oxide synthase (nNOS). Moreover, spinal GRPR+ neurons are gated by strong inhibitory inputs from the rostral ventromedial medulla. Thus, both local and long-range inhibitory inputs could play important roles in gating itch processing in the spinal cord by directly modulating the activity of spinal GRPR+ neurons.

SUBMITTER: Liu MZ 

PROVIDER: S-EPMC6936532 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Synaptic control of spinal GRPR<sup>+</sup> neurons by local and long-range inhibitory inputs.

Liu Ming-Zhe MZ   Chen Xiao-Jun XJ   Liang Tong-Yu TY   Li Qing Q   Wang Meng M   Zhang Xin-Yan XY   Li Yu-Zhuo YZ   Sun Qiang Q   Sun Yan-Gang YG  

Proceedings of the National Academy of Sciences of the United States of America 20191205 52


Spinal gastrin-releasing peptide receptor-expressing (GRPR<sup>+</sup>) neurons play an essential role in itch signal processing. However, the circuit mechanisms underlying the modulation of spinal GRPR<sup>+</sup> neurons by direct local and long-range inhibitory inputs remain elusive. Using viral tracing and electrophysiological approaches, we dissected the neural circuits underlying the inhibitory control of spinal GRPR<sup>+</sup> neurons. We found that spinal galanin<sup>+</sup> GABAergic n  ...[more]

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