Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Here we report the remodelling of neural networks which are likely to be the consequences of the segmental defect in the anterior forebrain of an animal model of Attention-Deficit Hyperactivity Disorder (ADHD), the juvenile prehypertensive male SHR rat. Molecular biology and microscope imaging techniques were used such as (i) dopamine (DA) D-1 and D-2 receptors by radioligand binding studies, (ii) the Ca2+/Calmoduhn-dependent protein kinase II, (CaMKII), (iii) transcription factors (TF) such as c-FOS, JUN-B and ZIF1/268 by ICC, and (iv) the respiratory chain enzyme cytochrome oxidase (C.O.), as markers of neuronal activity in the anterior forebrain of SHR and WKY controls. Microcomputer-assisted high-resolution image analysis revealed an altered cross talk within the amygdala complex in the SHR by CaMKII and c-FOS expression. In addition, cross-correlations among different regions within brain revealed an altered cross-talk in the forebrain of the SHR as compared to the controls using DA receptor binding and C.O, as probes. Therefore, the hypothesized segmental defect in the anterior forebrain of the SHR translates into network consequences explaining the attentional and hyperactivity main symptoms of ADHD as well as the emotional problems observed in a substantial number of cases of ADHD children. (Supported by Telethon-Italy grant E.513).

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Presentation Number SApapa0484
Keywords: ADHD, Attention, CaMKII, c-FOS, Neuronal Networks