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Dopamine (DA) strongly modulates the activity of neuronal ensembles in the prefrontal cortex. Activity of D1-like receptors, produced by phasic DA release, produces a net depressing effect by stimulating inhibitory interneurons, while on the other hand it enhances the activity levels of pyramidal cells that are strongly active. This produces an increase in the signal-to-noise ratio and contributes to the maintenance of behaviorally relevant circuits such as attentional systems and working memory ensembles. On the other hand, at much lower concentrations, D2-receptor-like activity produces a general disinhibition of cortical networks, favoring the maintenance of multiple representations and contributing to updating representations according to contextual changes. The balance between these two DA signaling systems is crucial, as failure to maintain the behavioral goal results in distractibility, while failure to update it with new sensory evidence results in perseverance. Thus, the mesencephalic DA system is a strong modulator of forebrain neurodynamics, both cortical and subcortical. A disbalance in the DA signaling systems might be one of the physiopathological mechanisms underlying neuropsychiatric disorders such as schizophrenia and attention deficit—hyperactivity disorder.

DOI: 10.1007/978-3-540-70573-4_11

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