期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 292, 期 5, 页码 C1768-C1774出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00440.2006
关键词
visceral pain; dorsal root ganglion neurons; acid-sensing ion channel; capsaicin receptor; acid-evoked currents; transient receptor potential vanilloid receptor 1
资金
- NINDS NIH HHS [NS-19912] Funding Source: Medline
Extracellular acidification contributes to pain by activating or modulating nociceptor activity. To evaluate acidic signaling from the colon, we characterized acid-elicited currents in thoracolumbar ( TL) and lumbosacral ( LS) dorsal root ganglion ( DRG) neurons identified by content of a fluorescent dye ( DiI) previously injected into the colon wall. In 13% of unidentified LS DRG neurons ( not labeled with DiI) and 69% of LS colon neurons labeled with DiI, protons activated a sustained current that was significantly and reversibly attenuated by the transient receptor potential vanilloid receptor 1 ( TRPV1) antagonist capsazepine. In contrast, 63% of unidentified LS DRG neurons and 4% of LS colon neurons exhibited transient amiloride- sensitive acid- sensing ion channel ( ASIC) currents. The peak current density of acid- elicited currents was significantly reduced in colon sensory neurons from TRPV1- null mice, supporting predominant expression of TRPV1 in LS colon sensory neurons, which was also confirmed immunohistochemically. Similar to LS colon DRG neurons, acid- elicited currents in TL colon DRG neurons were mediated predominantly by TRPV1. However, the pH producing half- activation of responses significantly differed between TL and LS colon DRG neurons. The properties of acid- elicited currents in colon DRG neurons suggest differential contributions of ASICs and TRPV1 to colon sensation and likely nociception.
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