REDUCED CAMKII-POSITIVE NEURONS IN THE ACCUMBENS SHELL OF AN ANIMAL-MODEL OF ATTENTION-DEFICIT HYPERACTIVITY DISORDER

ThIS study aimed at investigating putative neural substrates of attent ion-deficit hyperactivity disorder in children using the spontaneously hypertensive rat (SHR) as animal model and the Ca2+/calmodulin-depend ent protein kinase II (CaMKII) as a marker in the nucleus accumbens, a n interface between limbic and motor systems. In prehypertensive male SHR and Wistar-Kyoto rats image analysis of CaMKII immunocytochemistry showed more positive elements in the shell than in the core, and in t he former a lower level in SHR. The data indicate a reduced number of nucleus accumbens modules available for limbic-motor integration revea ling putative substrates of the altered attentional and reinforcement mechanisms demonstrated in the SHR and in children with attention-defi cit hyperactivity disorder.