Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.

Substance P (SP) and its receptor, the neurokinin 1 receptor (NK1R), play important roles in transmitting and regulating somatosensory nociceptive information. However, their roles in visceral nociceptive transmission and regulation remain to be elucidated. In the previous study, moderate SP immunor...

Full description

Bibliographic Details
Main Authors: Ming-Ming Zhang, Wei Ji, Li-Yu Pei, Wen Wang, Tao Chen, Wei Wang, Hui Li, Ting Zhang, Sheng-Xi Wu, Yun-Qing Li
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3605455?pdf=render
_version_ 1818509797863981056
author Ming-Ming Zhang
Wei Ji
Li-Yu Pei
Wen Wang
Tao Chen
Wei Wang
Hui Li
Ting Zhang
Sheng-Xi Wu
Yun-Qing Li
author_facet Ming-Ming Zhang
Wei Ji
Li-Yu Pei
Wen Wang
Tao Chen
Wei Wang
Hui Li
Ting Zhang
Sheng-Xi Wu
Yun-Qing Li
author_sort Ming-Ming Zhang
collection DOAJ
description Substance P (SP) and its receptor, the neurokinin 1 receptor (NK1R), play important roles in transmitting and regulating somatosensory nociceptive information. However, their roles in visceral nociceptive transmission and regulation remain to be elucidated. In the previous study, moderate SP immunoreactive (SP-ir) terminals and NK1R-ir neurons were observed in the dorsal commissural nucleus (DCN) of the lumbosacral spinal cord. Thus we hypothesized that the SP-NK1R system is involved in visceral pain transmission and control within the DCN. The acute visceral pain behaviors, the colon histological changes and the temporal and spatial changes of NK1R-ir structures and Fos expression in the neurons of the DCN were observed in rats following lower colon instillation with 5% formalin. The formalin instillation induced significant acute colitis as revealed by the histological changes in the colon. NK1R internalization in the DCN was obvious at 8 min. It reached a peak (75.3%) at 30 min, began to decrease at 90 min (58.1%) and finally reached the minimum (19.7%) at 3 h after instillation. Meanwhile, formalin instillation induced a biphasic visceral pain response as well as a strong expression of Fos protein in the nuclei of neurons in the DCN. Finally, intrathecal treatment with the NK1R antagonist L732138 attenuated the NK1R internalization, Fos expression and visceral nociceptive responses. The present results suggest that the visceral nociceptive information arising from inflamed pelvic organs, such as the lower colon, might be mediated by the NK1R-ir neurons in the DCN of the lumbosacral spinal cord.
first_indexed 2024-12-10T22:50:22Z
format Article
id doaj.art-4c8541aa434a497dab56e6c548470ff6
institution Directory Open Access Journal
issn 1932-6203
language English
last_indexed 2024-12-10T22:50:22Z
publishDate 2013-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS ONE
spelling doaj.art-4c8541aa434a497dab56e6c548470ff62022-12-22T01:30:26ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0183e5923410.1371/journal.pone.0059234Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.Ming-Ming ZhangWei JiLi-Yu PeiWen WangTao ChenWei WangHui LiTing ZhangSheng-Xi WuYun-Qing LiSubstance P (SP) and its receptor, the neurokinin 1 receptor (NK1R), play important roles in transmitting and regulating somatosensory nociceptive information. However, their roles in visceral nociceptive transmission and regulation remain to be elucidated. In the previous study, moderate SP immunoreactive (SP-ir) terminals and NK1R-ir neurons were observed in the dorsal commissural nucleus (DCN) of the lumbosacral spinal cord. Thus we hypothesized that the SP-NK1R system is involved in visceral pain transmission and control within the DCN. The acute visceral pain behaviors, the colon histological changes and the temporal and spatial changes of NK1R-ir structures and Fos expression in the neurons of the DCN were observed in rats following lower colon instillation with 5% formalin. The formalin instillation induced significant acute colitis as revealed by the histological changes in the colon. NK1R internalization in the DCN was obvious at 8 min. It reached a peak (75.3%) at 30 min, began to decrease at 90 min (58.1%) and finally reached the minimum (19.7%) at 3 h after instillation. Meanwhile, formalin instillation induced a biphasic visceral pain response as well as a strong expression of Fos protein in the nuclei of neurons in the DCN. Finally, intrathecal treatment with the NK1R antagonist L732138 attenuated the NK1R internalization, Fos expression and visceral nociceptive responses. The present results suggest that the visceral nociceptive information arising from inflamed pelvic organs, such as the lower colon, might be mediated by the NK1R-ir neurons in the DCN of the lumbosacral spinal cord.http://europepmc.org/articles/PMC3605455?pdf=render
spellingShingle Ming-Ming Zhang
Wei Ji
Li-Yu Pei
Wen Wang
Tao Chen
Wei Wang
Hui Li
Ting Zhang
Sheng-Xi Wu
Yun-Qing Li
Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.
PLoS ONE
title Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.
title_full Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.
title_fullStr Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.
title_full_unstemmed Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.
title_short Acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord.
title_sort acute colitis induces neurokinin 1 receptor internalization in the rat lumbosacral spinal cord
url http://europepmc.org/articles/PMC3605455?pdf=render
work_keys_str_mv AT mingmingzhang acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT weiji acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT liyupei acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT wenwang acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT taochen acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT weiwang acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT huili acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT tingzhang acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT shengxiwu acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord
AT yunqingli acutecolitisinducesneurokinin1receptorinternalizationintheratlumbosacralspinalcord