Autoradiographic analysis of rat brain kinin B1 and B2 receptors: normal distribution and alterations induced by epilepsy.

Kindling-induced seizures constitute an experimental model of human temporal lobe epilepsy that is associated with changes in the expression of several inflammatory proteins and/or their receptors in distinct brain regions. In the present study, alterations of kinin receptors in the brain of amygdaloid-kindled rats were assessed by means of in vitro autoradiography, using (125)I-labeled 3-4 hydroxyphenyl-propionyl-desArg(9)-D-Arg degrees -[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-bradykinin (B(1) receptors) and (125)I-labeled 3-4 hydroxyphenyl-propionyl-D-Arg degrees -[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-bradykinin (B(2) receptors) as ligands. Results demonstrate that B(2) receptors are widely distributed throughout the brain of control rats. The highest densities were observed in lateral septal nucleus, median preoptic nucleus, dentate gyrus, amygdala, spinal trigeminal nucleus, mediovestibular nucleus, inferior cerebellar peduncles, and in most of cortical regions (0.81-1.4 fmol/mg tissue). In contrast, very low densities of B(1) receptors were detected in all analyzed areas from control rats (0.18-0.26 fmol/mg tissue). When assessed in kindled rats, specific binding sites for B(2) receptors were significantly decreased (41 to 76%) in various brain areas. Conversely, B(1) receptor binding sites were markedly increased in kindled rats, especially in hippocampus (CA2 congruent with CA1 congruent with CA3), Amy and entorhinal, peririnal/piriform, and occipital cortices (152-258%). Data show for the first time that kindling-induced epilepsy results in a significant decline of B(2) receptor binding sites, accompanied by a striking increase of B(1) receptor labeling in the rat brain. An altered balance between B(1) and B(2) receptor populations may play a pivotal role in the onset and/or maintenance of epilepsy.