Abstract

Glycine receptors (GlyRs) are the main inhibitory chloride channels that control the excitability of spinal cord. Plastic changes in the excitability of peripheral and central nociceptive pathways accounts for development of chronic pain. Previous studies have shown the relevance of α3 homomeric GlyRs in pain sensitization induced by spinal PGE2 inflammation. A limited number of works have investigated the allosteric modulation of heteropentameric αβ GlyRs. Recently, we have published that homomeric GlyRs are more sensitive to the effects of ethanol and G protein therefore, β subunit may be negatively modulating α1β pharmacological profile in response to ethanol (Mariqueo et al., 2014). Considering the pharmacologic potential of this modulation, the present study examines the expression of β subunit in a rat neuropathic chronic pain model (CCI). Western blot analysis of spinal cord samples showed that β subunit expression increased in comparison with the control (Sham), after 3 days of pain development (mean ± SEM relative density 18±1 and 28±1 in the Sham and CCI slices, respectively, P˂0.05, n=2). Similar results were observed by immunofluorescence of β subunit in spinal slices (mean ± SEM Fluorescence arbitrary units 15.6 ± 1 and 47.6 ± 2, in the Sham and CCI slices, respectively, P˂0.001, n=4). Quantitative PCR showed increased level of β gene expression at 10 days after CCI surgery (2.2 fold, P˂0.001, n=3). These results highlight the importance of determining the role of β subunit in allosteric modulation of glycine receptors as a strategy against chronic pain process.