Imbalance Between Excitatory and Inhibitory Synaptic Transmission in the Primary Somatosensory Cortex Caused by Persistent Nociception in Rats

JOURNAL OF PAIN

卷:20

Article

Cao, Fa-Le^1,2,3  Xu, Min⁴  Gong, Kerui⁵  Wang, Yan^2,3  Wang, Ruirui^2,3  Chen, Xuefeng^2,3  Chen, Jun^2,3 

[1] 88th Hosp PLA, Dept Neurol, Tai An, Shandong, Peoples R China

[2] Fourth Mil Med Univ, Tangdu Hosp, Inst Biomed Sci Pain, 1 Xinsi Rd, Xian 710038, Shaanxi, Peoples R China

[3] Fourth Mil Med Univ, Tangdu Hosp, Inst Funct Brain Disorders, 1 Xinsi Rd, Xian 710038, Shaanxi, Peoples R China

[4] 88th Hosp PLA, Dept Nephrol, Tai An, Shandong, Peoples R China

[5] Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA

关键词: Primary somatosensory cortex;    synaptic plasticity;    AMPA receptor;    GABA receptor;    bee venom test;    multi-electrode array;   

DOI  :  10.1016/j.jpain.2018.11.014

来源: Elsevier

【 摘 要 】

There is substantial evidence supporting the notion that the primary somatosensory (Si) cortex is an important structure involved in the perceptional component of pain. However, investigations have mainly focused on other pain-related formations, and few reports have been provided to investigate the synaptic plasticity in the S1 cortex in response to persistent pain. In the present study, we report that bee venom (BV) injection triggered an imbalance between excitatory and inhibitory synaptic transmission in the S1 cortex in rats. Using a multi-electrode array recording, we found that BV-induced persistent inflammatory pain led to temporal and spatial enhancement of synaptic plasticity. Moreover, slice patch clamp recordings on identified pyramidal neurons demonstrated that BV injection increased presynaptic and postsynaptic transmission in excitatory synapses and decreased postsynaptic transmission in inhibitory synapses in the layer II/III neurons within the S1 cortex. In immunohistochemistry and Western blot sections, the distribution and expression of total AMPA receptor subunits and gamma-amino butyric acid-A (GABAA) were unaffected, although the membrane fractions of GluR2 and GABA(A) were decreased, and their cytosolic fractions were increased in contrast. The change of GluR1 was opposite to that of GluR2, and GIuR3 did not change significantly. Our studies, therefore, provide direct evidence for both presynaptic and postsynaptic changes in synapses within the S1 cortex in persistent nociception, which are probably related to the membrane trafficking of GluR1, GluR2, and GABA(A). Perspective: Increased synaptic plasticity was detected in S1 after peripheral nociception, with enhanced excitatory and decreased inhibitory synaptic transmissions. Increased GluR1, and decreased GABA(A)alpha 1 and GluR2 membrane trafficking were detected. Therefore, the disrupted excitatory/inhibitory balance in transmissions is in in nociception processing, and S1 can be a potential antinociceptive site. (C) 2019 by the American Pain Society

【 授权许可】

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