期刊
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
卷 306, 期 9, 页码 G788-G795出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00318.2013
关键词
tumor necrosis factor-alpha; satellite glial cells
资金
- National Nature Science Foundation of China [81070303, 81170347]
Communication between neurons and glia in the dorsal root ganglia (DRG) and the central nervous system is critical for nociception. Both glial activation and proinflammatory cytokine induction underlie this communication. We investigated whether satellite glial cell (SGC) and tumor necrosis factor-alpha (TNF-alpha) activation in DRG participates in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat model of visceral hyperalgesia. In TNBS-treated rats, TNF-alpha expression increased in DRG and was colocalized to SGCs enveloping a given neuron. These SGCs were activated as visualized under electron microscopy: they had more elongated processes projecting into the connective tissue space and more gap junctions. When nerves attached to DRG (L-6-S-1) were stimulated with a series of electrical stimulations, TNF-alpha were released from DRG in TNBS-treated animals compared with controls. Using a current clamp, we noted that exogenous TNF-alpha (2.5 ng/ml) increased DRG neuron activity, and visceral pain behavioral responses were reversed by intrathecal administration of anti-TNF-alpha (10 mu g center dot kg(-1)center dot day(-1)). Based on our findings, TNF-alpha and SGC activation in neuron-glial communication are critical in inflammatory visceral hyperalgesia.
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