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 125I-labeled 3-4 hydroxyphenyl-propionyl-desArg9-D-Arg°-[Hyp3, Thi5, D-Tic7, Oic8]-bradykinin (B1 receptors) and 125I-labeled 3-4 hydroxyphenyl-propionyl-D-Arg°[Hyp3, Thi5, D-Tic7, Oic8]-bradykinin (B2 receptors) as ligands. Results demonstrate that B2 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 B1 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 B2 receptors were significantly decreased (41 to 76%) in various brain areas. Conversely, B1 receptor binding sites were markedly increased in kindled rats, especially in hippocampus (CA2 ≅ CA1 ≅ 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 B2 receptor binding sites, accompanied by a striking increase of B1 receptor labeling in the rat brain. An altered balance between B1 and B2 receptor populations may play a pivotal role in the onset and/or maintenance of epilepsy. © 2003 Wiley-Liss, Inc.
Autoradiographic analysis of rat brain kinin B-1 and B-2 receptors: Normal distribution and alterations induced by epilepsy
BREGOLA, Gianni;RODI, Donata;REGOLI, Domenico;SIMONATO, Michele;
2003
Abstract
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 125I-labeled 3-4 hydroxyphenyl-propionyl-desArg9-D-Arg°-[Hyp3, Thi5, D-Tic7, Oic8]-bradykinin (B1 receptors) and 125I-labeled 3-4 hydroxyphenyl-propionyl-D-Arg°[Hyp3, Thi5, D-Tic7, Oic8]-bradykinin (B2 receptors) as ligands. Results demonstrate that B2 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 B1 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 B2 receptors were significantly decreased (41 to 76%) in various brain areas. Conversely, B1 receptor binding sites were markedly increased in kindled rats, especially in hippocampus (CA2 ≅ CA1 ≅ 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 B2 receptor binding sites, accompanied by a striking increase of B1 receptor labeling in the rat brain. An altered balance between B1 and B2 receptor populations may play a pivotal role in the onset and/or maintenance of epilepsy. © 2003 Wiley-Liss, Inc.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
