GABAB receptor activation attenuates inflammatory orofacial pain by modulating interleukin-1 β in satellite glial cells: role of NF-κB and MAPK signaling pathways.

The objective of this study was to investigate whether GABAB receptors in TG SGCs attenuate inflammatory facial pain via mediating IL-1β following inflammation and its mechanisms. Complete Freund's adjuvant (CFA) was injected into the whisker pad of rats to induce inflammation in vivo. Lipopolysaccharide (LPS) was added to culture medium to activate SGCs in vitro. Behavioral measures showed that microinjection of baclofen (a selective GABAB receptor agonist) into the TG ameliorated the mechanical allodynia of CFA-treated rats. Interestingly, baclofen pretreatment inhibited SGC activation and IL-1β production, however, preserved the decreased expression of GABAB receptors in SGCs activated by CFA in vivo and LPS in vitro. In addition, baclofen suppressed the increased expression of p-NF- κ B p65, p-I κ Bα, and p-p38 MAPK, while reversed the decreased production of I κ Bα, and further enhanced the increased expression of p-ERK(1/2) in LPS-treated SGCs in vitro. Finally, those effects of baclofen were abolished by saclofen (a specific GABAB receptor antagonist) co-administration. Altogether, these results demonstrated for the first time that activation of GABAB receptor might inhibit IL-1β production by suppressing NF- κ B and p38 MAPK signaling pathway activation and restore GABAB receptor expression in SGCs to attenuate inflammatory facial pain. PMID: 31034945 [PubMed - as supplied by publisher]
Source: Brain Research Bulletin - Category: Neurology Authors: Tags: Brain Res Bull Source Type: research

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Source: Neuromodulation: Technology at the Neural Interface - Category: Biotechnology Authors: Tags: Case Series Source Type: research
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Source: NeuroReport - Category: Neurology Tags: Cellular, Molecular and Developmental Neuroscience Source Type: research
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