Expression and distribution of kinin B 1 receptor in the rat brain and alterations induced by diabetes in the model of streptozotocin

A role for kinin B 1 receptors was suggested in the spinal cord and peripheral organs of streptozotocin (STZ)‐diabetic rats. The present study aims at determining whether B 1 receptors are also induced and over‐expressed in the brain of STZ‐rats at 2, 7, and 21 days post‐treatment. This was addressed by in situ hybridization using the [ 35 S]‐UTPαS‐labeled riboprobe and by in vitro autoradiography with the radioligand [ 125 I]‐HPP‐des‐Arg 10 ‐Hoe 140. In control rats, B 1 receptor mRNA was found widely distributed in many brain regions. Low mRNA levels were found in thalamus and hypothalamus (7–12 nCi/g) while high mRNA signals were detected in cortical regions and hippocampus (18–29 nCi/g). In diabetic rats, B 1 receptor mRNA was markedly increased in hippocampus, temporal/parietal cortices and amygdala at 2 and 7 days (+88 to +150%). Low densities of B 1 receptor binding sites were detected in all analyzed regions in control rats (0.18–0.37 fmol/mg tissue). In diabetic rats, B 1 receptor binding sites were significantly increased in hippocampus, amygdala, temporal/parietal, and perhinal/piriform cortices (+ 55 to + 165 %) at 7 days only. Results highlight an early but transient and reversible up‐regulation of B 1 receptors in specific brain regions of STZ‐diabetic rats. This may offer the advantage of reducing putative central side effects with B 1 receptor antagonists if used for the treatment of diabetic complications in the periphery. Synapse 57:29–37, 2005. © 2005 Wiley‐Liss, Inc.