Elevated interleukin-8 enhances prefrontal synaptic transmission in mice with persistent inflammatory painReport as inadecuate




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Molecular Pain

, 8:11

First Online: 12 February 2012Received: 30 November 2011Accepted: 12 February 2012

Abstract

BackgroundInterleukin-8 IL-8 is known for its roles in inflammation and plays critical roles in the development of pain. Its expression increases in the brain after peripheral inflammation. Prefrontal cortex, including the anterior cingulate cortex ACC, is a forebrain structure known for its roles in pain transmission and modulation. Painful stimuli potentiate the prefrontal synaptic transmission, however, little is known about the expression of IL-8 and its role in the enhanced ACC synaptic transmission in animals with persistent inflammatory pain.

FindingsIn the present study, we examined IL-8 expression in the ACC, somatosensory cortex SSC, and the dorsal horn of lumbar spinal cord following hind-paw administration of complete Freund-s adjuvant CFA in mice and its effects on the ACC synaptic transmission. Quantification of IL-8 at protein level by ELISA revealed enhanced expression in the ACC and spinal cord during the chronic phases of CFA-induced peripheral inflammation. In vitro whole-cell patch-clamp recordings revealed that IL-8 significantly enhanced synaptic transmission through increased probability of neurotransmitter release in the ACC slice. ACC local infusion of repertaxin, a non-competitive allosteric blocker of IL-8 receptors, notably prolonged the paw withdrawal latency to thermal radian heat stimuli bilaterally in mice.

ConclusionsOur findings suggest that up-regulation of IL-8 in the ACC partly attributable to the enhanced prefrontal synaptic transmission in the mice with persistent inflammatory pain.

KeywordsInterleukin-8 Inflammation Pain Cingulate cortex Electronic supplementary materialThe online version of this article doi:10.1186-1744-8069-8-11 contains supplementary material, which is available to authorized users.

Guang-bin Cui, Jia-ze An contributed equally to this work.

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Author: Guang-bin Cui - Jia-ze An - Nan Zhang - Ming-gao Zhao - Shui-bing Liu - Jun Yi

Source: https://link.springer.com/







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