Cerebrospinal fluid-contacting nucleus mediates nociception via release of fractalkine.

Abstract

Increasing evidence suggests that the cerebrospinal fluid-contacting nucleus (CSF-contacting nucleus) mediates the transduction and regulation of pain signals. However, the precise molecular mechanisms remain unclear. Studies show that release of fractalkine (FKN) from neurons plays a critical role in nerve injury-related pain. We tested the hypothesis that release of FKN from the CSF-contacting nucleus regulates neuropathic pain, in a chronic constriction injury rat model. The results show that FKN is expressed by neurons, via expression of its only receptor CX3CR1 in the microglia. The levels of soluble FKN (sFKN) were markedly upregulated along with the increase in FKN mRNA level in rats subjected to chronic constriction injury. In addition, injection of FKN-neutralizing antibody into the lateral ventricle alleviated neuropathic pain-related behavior followed by reduction in microglial activation in the CSF-contacting nucleus. The results indicate that inhibition of FKN release by the CSF-contacting nucleus may ameliorate neuropathic pain clinically.

• Authors: Q Q Zhou, S S Chen, Q Q Zhang, P F Liu, H Z Fang, Y Yang, L C Zhang
• Journal: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas (Braz J Med Biol Res) Vol. 50 Issue 9 Pg. e6275 (Aug 07 2017) ISSN: 1414-431X [Electronic] Brazil
• PMID: 28793053 (Publication Type: Journal Article)

Chemical References

• Chemokine CX3CL1

Topics

• Animals
• Cell Nucleus (metabolism)
• Cerebrospinal Fluid (metabolism)
• Chemokine CX3CL1 (metabolism)
• Chronic Pain (metabolism)
• Disease Models, Animal
• Injections, Intraventricular
• Male
• Neuralgia (metabolism)
• Pain Threshold (physiology)
• Rats
• Rats, Sprague-Dawley
• Up-Regulation