Reduced CaMKII-positive neurones in the accumbens shell of an animal model of attention-deficit hyperactivity disorder.
THIS study aimed at investigating putative neural substrates of attention-deficit hyperactivity disorder in children using the spontaneously hypertensive rat (SHR) as animal model and the Ca2+/calmodulin-dependent protein kinase II (CaMKII) as a marker in the nucleus accumbens, an 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 the former a lower level in SHR. The data indicate a reduced number of nucleus accumbens modules available for limbic-motor integration revealing putative substrates of the altered attentional and reinforcement mechanisms demonstrated in the SHR and in children with attention-deficit hyperactivity disorder.
Papa
M
M
Institute of Human Anatomy, Second University of Naples (SUN), Italy.
Sagvolden
T
T
Sergeant
J A
JA
Sadile
A G
AG
D000818:Animals; D001288:Attention / Q000502:physiology; D001289:Attention Deficit Disorder with Hyperactivity / Q000201:enzymology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000096:biosynthesis / Q000378:metabolism*; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000096:biosynthesis / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000201:enzymology*; D009714:Nucleus Accumbens / Q000166:cytology / Q000201:enzymology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
D007527:Isoenzymes; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases