Behavioural, pharmacological, morpho-functional molecular studies reveal a hyperfunctioning mesocortical dopamine system in an animal model of attention deficit and hyperactivity disorder

Midbrain Dopamine Neurons: Projection Target Determines Action Potential Duration and Dopamine D2Receptor Inhibition

“…It is possible that such neurons have firing patterns distinct from those of NAc-projecting DA neurons. In view of the critical roles of DA release in a variety of important functions including working memory (Phillips et al, 2008), learning, motivation, and reinforcement (Fields et al, 2007), and that the dysfunction of midbrain DA neurons contributes to disease states such as schizophrenia (Sesack and Carr, 2002), attention deficit hyperactivity disorder (Viggiano et al, 2003), and drug addiction (Lüs-cher and Ungless, 2006), it is essential that we have a more complete understanding of the firing patterns of all classes of VTA DA neurons. Here we show that determining the projection target of VTA neurons increases the accuracy of DA neuron identification in addition to the inherent value of knowing the connectivity of the neuron in question.…”

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

“…This increased activity is dependent on the environment, e.g. no hyperactivity could be observed in the rats' home cage (Sadile 1993) and motor activity increased with increasing complexity of the environment Viggiano et al 2002bViggiano et al , 2003b. In addition, NHE rats showed deficits in visual-spatial attention but no deficits in working memory (Aspide et al 1998;Gallo et al 2002;Papa et al 2000).…”

Possible involvement of alpha‐2A adrenergic receptors in attention deficit hyperactivity disorder: Radioligand binding and polymorphism studies

“…Animal studies have implicated the catecholamine neurotransmitters (norepinephrine, epinephrine, and dopamine) in the modulation of attention, hyperactivity, and impulse control [Jones and Hess, 2003;Leo et al, 2003;Viggiano et al, 2003Viggiano et al, , 2004. Neurobiological and pharmacological research has focused attention on dysregulation of the catecholamine systems in the pathophysiology of ADHD [Pliszka et al, 1996].…”

“…Neurobiological and pharmacological research has focused attention on dysregulation of the catecholamine systems in the pathophysiology of ADHD [Pliszka et al, 1996]. It has been hypothesized that ADHD may be the result of an imbalance between the norepinephrine and dopamine systems in the prefrontal cortex, with extracellular norepinephrine enhancing dopamine release by activating the adrenergic receptors and extracellular dopamine increasing the extracellular levels of norepinephrine by activating the dopamine receptors [Arnsten, 2000;Viggiano et al, 2003Viggiano et al, , 2004. Recent technological developments of linkage and association methods have allowed researchers to identify candidate genes associated with these pathways [Ogdie et al, 2003[Ogdie et al, , 2004Bobb et al, 2004;Lowe et al, 2004].…”