Neurochemical research
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Neurochemical research · Apr 2015
Nonvesicular release of ATP from rat retinal glial (Müller) cells is differentially mediated in response to osmotic stress and glutamate.
Retinal glial (Müller) cells release ATP upon osmotic stress or activation of metabotropic glutamate receptors. ATP inhibits the osmotic Müller cell swelling by activation of P2Y1 receptors. In the present study, we determined the molecular pathways of the ATP release from Müller cells in slices of the rat retina. ⋯ The p-glycoprotein blocker verapamil had no effect. As revealed by single-cell RT-PCR, subpopulations of Müller cells expressed mRNAs for pannexin-1 and -2, and connexins 30, 30.3, 32, 43, 45, and 46. The data may suggest that rat Müller cells release ATP by multidrug resistance channels, CFTR, and connexin hemichannels in response to osmotic stress, while glutamate induces a release of ATP via multidrug resistance channels, connexin hemichannels, and pannexin-1.
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Neurochemical research · Apr 2015
IL-10 and IL-1β mediate neuropathic-pain like behavior in the ventrolateral orbital cortex.
Previous evidence has shown that the glial cells can be activated by peripheral nerve injury and release both pro-inflammatory and anti-inflammatory cytokines, which play crucial roles in the establishment and maintenance of neuropathic pain. The present study examined the roles of anti-inflammatory cytokine IL-10 and pro-inflammatory IL-1β on allodynia induced by spared nerve injury (SNI) in the ventrolateral orbital cortex (VLO) in the rat. The mechanical paw withdrawal threshold (PWT) was measured using von-Frey filaments. ⋯ Moreover, western blotting results showed expression levels of IL-10 and IL-1β significantly up-regulated in the contralateral VLO of SNI rats as compared with that of sham-operated rats. These results suggest that anti-inflammatory cytokine IL-10 and pro-inflammatory cytokine IL-1β mediate neuropathic-pain like behavior at the cerebral cortex level; IL-10 released from activated glial cells in the VLO can potentially attenuate allodynia while IL-1β released from activated glial cells in the VLO can potentially maintain or facilitate allodynia. These results provide new insights and site for therapy at the cerebral cortex level in neuropathic pain condition.