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阻断 BK 通道可减轻 IBS 样大鼠模型中的慢性内脏敏感性。

Blockade of BK channels attenuates chronic visceral hypersensitivity in an IBS-like rat model.

机构信息

Nursing Department, Fujian Health College, China.

School of basic Medical Sciences, Laboratory of Pain Research, Fujian Provincial Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Medical University, China.

出版信息

Mol Pain. 2021 Jan-Dec;17:17448069211040364. doi: 10.1177/17448069211040364.

DOI:10.1177/17448069211040364
PMID:34407673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8381452/
Abstract

BACKGROUND

Visceral hypersensitivity in irritable bowel syndrome (IBS) is still poorly understood, despite that chronic abdominal pain is the most common symptoms in IBS patients. To study effects of BK channels on visceral hypersensitivity in IBS rats and the underlying mechanisms, IBS rats were established by colorectal distention (CRD) in postnatal rats. The expression of large-conductance calcium and voltage-dependent potassium ion channels (BK channels) of the thoracolumbar spinal cord was examined in IBS and control rats. The effects of BK channel blockade on visceral hypersensitivity were evaluated. The interaction of BK channels and N-methyl-D-aspartate acid (NMDA) receptors was explored, and synaptic transmission at superficial dorsal horn (SDH) neurons of the thoracolumbar spinal cord was recorded by whole-cell patch clamp in IBS rats.

RESULTS

The expression of the BK channels of the thoracolumbar spinal cord in IBS rats was significantly reduced. The blockade of BK channels could reduce the visceral hypersensitivity in IBS rats. There was an interaction between BK channels and NMDA receptors in the spinal cord. The frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) in SDH neurons is significantly reduced in IBS rats. The blockade of BK channels depolarizes the inhibitory interneuron membrane and increases their excitability in IBS rats.

CONCLUSIONS

BK channels could interact with NMDA receptors in the thoracolumbar spinal cord of rats and regulate visceral hypersensitivity in IBS rats.

摘要

背景

尽管慢性腹痛是肠易激综合征（IBS）患者最常见的症状，但内脏敏感性仍然知之甚少。为了研究 BK 通道对 IBS 大鼠内脏敏感性的影响及其潜在机制，通过对新生大鼠进行结肠扩张（CRD）来建立 IBS 大鼠模型。在 IBS 和对照大鼠中检查了胸腰段脊髓中大电导钙和电压依赖性钾离子通道（BK 通道）的表达。评估了 BK 通道阻断对内脏敏感性的影响。探讨了 BK 通道与 N-甲基-D-天冬氨酸（NMDA）受体的相互作用，并通过全细胞膜片钳记录 IBS 大鼠胸腰段脊髓浅层背角（SDH）神经元的突触传递。

结果

IBS 大鼠胸腰段脊髓 BK 通道的表达明显减少。BK 通道阻断可降低 IBS 大鼠的内脏敏感性。脊髓中 BK 通道和 NMDA 受体之间存在相互作用。IBS 大鼠 SDH 神经元的自发性抑制性突触后电流（sIPSCs）频率明显降低。BK 通道阻断使抑制性中间神经元膜去极化，增加了 IBS 大鼠的兴奋性。

结论

BK 通道可在大鼠胸腰段脊髓中与 NMDA 受体相互作用，调节 IBS 大鼠的内脏敏感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/05a7c5cbabe1/10.1177_17448069211040364-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/680e8db0773f/10.1177_17448069211040364-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/3317b1883794/10.1177_17448069211040364-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/67fbedec5a46/10.1177_17448069211040364-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/30e3697a51af/10.1177_17448069211040364-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/79456041c5ad/10.1177_17448069211040364-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/589d5df9a040/10.1177_17448069211040364-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/05a7c5cbabe1/10.1177_17448069211040364-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/680e8db0773f/10.1177_17448069211040364-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/3317b1883794/10.1177_17448069211040364-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/67fbedec5a46/10.1177_17448069211040364-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/30e3697a51af/10.1177_17448069211040364-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/79456041c5ad/10.1177_17448069211040364-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/589d5df9a040/10.1177_17448069211040364-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6b3/8381452/05a7c5cbabe1/10.1177_17448069211040364-fig7.jpg

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