Invited Symposium: What Can Genetic Models Tell Us About Attention-Deficit Hyperactivity Disorder (ADHD)?
Molecular biology and microscope imaging techniques were used to map putative neural substrates of Attention-Deficit Hyperactivity Disorder (ADHD) in animal models such as the juvenile prehypertensive male SHR rat. The spatial distribution has been studied in nterior forebrain sections of HR and WKY controls for markers such as of (i) dopamine (DA) D-1 and D-2 receptor families by radioligand binding studies, (ii) the Ca2+/Calmoduhn-dependent protein kinase II (CaMKII), and (iii) transcription factors (TF) such as c-FOS, JUN-B and ZIF/268 by immunocytochemistry. Microcomputer-assisted high-resolution image analysis showed in the SHR a higher density of DA D-1 but not D-2 receptors paralleled by a reduced number of elements positive for CaMKII, TFs and C.O., which was restricted to the most rostral portions of the caudate-putarnen, the pole and shell of the n.accumbens. and the olfactory tubercle. The higher number of DA D- 1 binding sites is coherent with a reduced DA release leading to a reduced number of accumbal elements and modules available for limbic-motor integration in a specific, discrete segment of the anterior forebrain. This segmental defect was partially reversed by environmental stimulation and by subchronic treatment with a DA re-uptake blocker, methylphenidate, during the 5th and 6th postnatal week. The data are consistent with the genetic contribution as well as with the role of environmental factors in the phenotypic expression of ADHD. (Supported by Telethon-Italy grant E.513).
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|Sadile, AG; (1998). Segmental Defect in the Anterior Forebrain of an Animal Model of ADHD. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/sadile/sadile0504/index.html|
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