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Background  The kinin B 1  receptor (B 1 R) is upregulated by pro-inflammatory cytokines, bacterial endotoxins and hyperglycaemia-induced oxidative stress. In animal models of diabetes, it contributes to pain polyneuropathy. This study aims at defining the cellular localization of B 1 R in thoracic spinal cord of type 1 diabetic rats by confocal microscopy with the use of a fluorescent agonist, [Nα-Bodipy]-des-Arg 9 -BK (BdABK) and selective antibodies.    Methods  Diabetes was induced by streptozotocin (STZ; 65 mg/kg, i.p.). Four days post-STZ treatment, B 1 R expression was confirmed by quantitative real-time PCR and autoradiography. The B 1 R selectivity of BdABK was determined by assessing its ability to displace B 1 R [ 125 I]-HPP-desArg 10 -Hoe140 and B 2 R [ 125 I]-HPP-Hoe 140 radioligands. The  in vivo  activity of BdABK was also evaluated on thermal hyperalgesia.    Results  B 1 R was increased by 18-fold (mRNA) and 2.7-fold (binding sites) in the thoracic spinal cord of STZ-treated rats when compared to control. BdABK failed to displace the B 2 R radioligand but displaced the B 1 R radioligand (IC 50  = 5.3 nM). In comparison, IC 50  values of B 1 R selective antagonist R-715 and B 1 R agonist des-Arg 9 -BK were 4.3 nM and 19 nM, respectively. Intraperitoneal BdABK and des-Arg 9 -BK elicited dose-dependent thermal hyperalgesia in STZ-treated rats but not in control rats. The B 1 R fluorescent agonist was co-localized with immunomarkers of microglia, astrocytes and sensory C fibers in the spinal cord of STZ-treated rats.    Conclusion  The induction and up-regulation of B 1 R in glial and sensory cells of the spinal cord in STZ-diabetic rats reinforce the idea that kinin B 1 R is an important target for drug development in pain processes.

Cellular localization of kinin B1 receptor in the spinal cord of streptozotocin-diabetic rats with a fluorescent [Nα-Bodipy]-des-Arg9-bradykinin