UNASSIGNED: 6 Background: @entity1897 is a debilitating side effect and dose limiting @entity137 of anticancer drug therapies. @entity1897 induces pathological changes in dorsal root ganglia (DRG), leading to increased cross-talk between sensory neurons and satellite glial cells (SGCs), specifically @entity855 mediated SGC-neuron signaling. We therefore investigated @entity1897 in @entity19 with neuron- or glia-specific deletion of the @entity855 -releasing channel @entity18539 ( @entity18539 ). METHODS: To induce @entity1897 , @entity19 were given two i.p. @entity901 ( @entity15114 ) injections two days apart. Controls received saline (sal). We used C57Bl6 wildtype and @entity19 with neuron- or glia-specific @entity18539 deletion (NFHcre or GFAPcre:Panx1F/F) and littermate controls (Panx1F/F), 7-11 per group. Tactile sensitivity of the hindpaws was assessed prior to and every week after injections for 3 weeks using von Frey filaments. The number of paw withdrawals to 10 stimulations with each filament and @entity158 thresholds (corresponding to filament that elicits 8/10 responses) were recorded. Overall @entity19 condition was assessed using Open Field Tests. RESULTS: C57Bl6 @entity19 developed transient @entity56 after @entity15114 injection, which was most prominent at day 9 and ceased at day 21. @entity15114 -injected @entity19 had lower tactile thresholds (at 9 days: sal 5.5  0.3g vs. @entity15114 2.7  0.4g, p < 0.001) and higher response rates to filaments compared to sal-injected controls (p < 0.05), but revealed no changes in any other behavior. @entity19 with glia-specific @entity18539 deletion did not display significant @entity56 at any time after @entity15114 (tactile threshold at 9 days: sal 5.5  0.3g vs. @entity15114 5.8  0.2g), whereas @entity15114 induced @entity56 did occur in @entity19 with neuron-specific @entity18539 deletion (at 9 days: sal 6  0g vs. @entity15114 1.3  0g, p < 0.0001) and Panx1F/F littermates (at 9 days: sal 6.0  0g vs. @entity15114 1.3  0.1g, p < 0.0001). CONCLUSIONS: We found that @entity901 induces transient @entity1897 , but no other behavioral changes in wildtype @entity19 . Deletion of the @entity855 -releasing channel @entity18539 in glia, but not in neurons, prevented @entity1897 development. This points to a new molecule ( @entity18539 ) and a new cell type (glia) as potential novel targets for @entity158 therapy.

The role of @entity18539 in XXXX ( @entity1897 ).

@entity901 :: ('MESH:C030110', 'Chemical') :: ['oxaliplatin'] @entity137 :: ('MESH:D064420', 'Disease') :: ['toxicity'] @entity19 :: ('10090', 'Species') :: ['mice', 'mouse', 'transgenic mice', 'Mice'] @entity18539 :: ('55991(Tax:10090)', 'Gene') :: ['Panx 1', 'Pannexin 1', 'Panx1'] @entity15114 :: ('MESH:C015692', 'Chemical') :: ['Oxa', 'oxa'] @entity1897 :: ('MESH:D010523', 'Disease') :: ['CIPN'] @entity56 :: ('MESH:D004342', 'Disease') :: ['tactile hypersensitivity'] @entity158 :: ('MESH:D010146', 'Disease') :: ['pain'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity1897 :: (MESH:D010523,Disease) :: ['chemotherapy-induced peripheral neuropathy']
