Dopamine Neurotransmission and Atypical Antipsychotics in Prefrontal Cortex: A Critical Review
Schizophrenia has been historically characterized by the presence of positive symptomatology, however, decades
of research highlight the importance of cognitive deficits in this disorder. At present, cognitive impairments remain
one of the most important unmet therapeutic needs in schizophrenia. The prefrontal cortex (PFC) controls a large number
of higher brain functions altered in a variety of psychiatric disorders, including schizophrenia. Histological studies indicate
the presence of a large proportion of PFC neurons expressing monoaminergic receptors sensitive to the action of current
atypical antipsychotics. Functional studies also show that these medications act at PFC level to increase dopamine
neurotransmission in the mesocortical pathway. Here we focus on monoaminergic molecular targets that are actively being
explored as potential therapeutic agents in the basic and clinical cognitive neuroscience research, to support the development
of co-treatments used in conjunction with antipsychotic medications. These targets include dopamine and serotonin
receptors in the prefrontal cortex, as well as elements of the noradrenergic system.
Keywords: Antipsychotic drugs, cognitive deficits, monoamines, prefrontal cortex, schizophrenia.
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