BACKGROUND: @entity460 -activated @entity2865 channels (CaCCs) activation induces membrane depolarization by increasing @entity2865 efflux in primary sensory neurons that can facilitate action potential generation. Previous studies suggest that CaCCs family members @entity69388 and anoctamin-1 are involved in @entity158 . However, their role in @entity9 is unclear. In this investigation we assessed the involvement of these CaCCs family members in @entity35 subjected to the L5/L6 spinal nerve ligation. In addition, anoctamin-1 and @entity69388 mRNA and protein expression in dorsal root ganglion (DRG) and spinal cord was also determined in the presence and absence of selective inhibitors. RESULTS: L5/L6 spinal nerve ligation induced mechanical tactile @entity1931 . Intrathecal administration of non-selective CaCCs inhibitors ( @entity18107 , 9-AC and NFA) dose-dependently reduced tactile @entity1931 . Intrathecal administration of selective CaCCs inhibitors (T16Ainh-A01 and CaCCinh-A01) also dose-dependently diminished tactile @entity1931 and thermal @entity1931 . Anoctamin-1 and @entity69388 mRNA and protein were expressed in the dorsal spinal cord and DRG of na  ve, sham and neuropathic @entity35 . L5/L6 spinal nerve ligation rose mRNA and protein expression of anoctamin-1, but not @entity69388 , in the dorsal spinal cord and DRG from day 1 to day 14 after nerve ligation. In addition, repeated administration of CaCCs inhibitors (T16Ainh-A01, CaCCinh-A01 or NFA) or anti-anoctamin-1 antibody prevented spinal nerve ligation-induced rises in anoctamin-1 mRNA and protein expression. Following spinal nerve ligation, the compound action potential generation of putative C fibers increased while selective CaCCs inhibitors (T16Ainh-A01 and CaCCinh-A01) attenuated such increase. CONCLUSIONS: There is functional anoctamin-1 and @entity69388 expression in @entity35 at sites related to nociceptive processing. Blockade of these CaCCs suppresses compound action potential generation in putative C fibers and lessens established tactile @entity1931 . As CaCCs activity contributes to @entity9 maintenance, selective inhibition of their activity may function as a tool to generate analgesia in nerve @entity158 states.

Role of anoctamin-1 and XXXX in spinal nerve ligation-induced @entity9 in @entity35 .

@entity1931 :: ('MESH:D006930', 'Disease') :: ['allodynia', 'hyperalgesia'] @entity69388 :: ('293735(Tax:10116)', 'Gene') :: ['bestrophin-1'] @entity2865 :: ('CHEBI:17996', 'Chemical') :: ['chloride'] @entity158 :: ('MESH:D010146', 'Disease') :: ['inflammatory pain', 'injury pain'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['Calcium'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity9 :: ('MESH:D009437', 'Disease') :: ['neuropathic pain'] @entity18107 :: ('25105(Tax:10116)', 'Gene') :: ['NPPB']
@entity69388 :: (293735(Tax:10116),Gene) :: ['bestrophin-1']
