Acta psychiatrica Scandinavica · 2010
The prefrontal cortex: a target for antipsychotic drugs.
СтатьяПоддержка исследования: вне правительства СШАОбзорНазвание и аннотация: Перевод в очереди
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Аннотация
OBJECTIVE: At therapeutic doses, classical antipsychotic drugs occupy a large proportion of subcortical dopamine D2 receptors, whereas atypical antipsychotics preferentially occupy cortical 5-HT(2) receptors. However, the exact cellular and network basis of their therapeutic action is not fully understood.
METHOD: To review the mechanism of action of antipsychotic drugs with a particular emphasis on their action in the prefrontal cortex (PFC).
RESULTS: The PFC controls a large number of higher brain functions altered in schizophrenia. Histological studies indicate the presence of a large proportion of PFC neurons expressing monoaminergic receptors sensitive to the action of atypical- and to a lesser extentclassical antipsychotic drugs. Functional studies also indicate that both drug families act at PFC level.
CONCLUSION: Atypical antipsychotic drugs likely exert their therapeutic activity by a preferential action on PFC neurons, thus modulating the PFC output to basal ganglia circuits. Classical antipsychotics also interact with these PFC targets in addition to blocking massively striatal D2 receptors.
METHOD: To review the mechanism of action of antipsychotic drugs with a particular emphasis on their action in the prefrontal cortex (PFC).
RESULTS: The PFC controls a large number of higher brain functions altered in schizophrenia. Histological studies indicate the presence of a large proportion of PFC neurons expressing monoaminergic receptors sensitive to the action of atypical- and to a lesser extentclassical antipsychotic drugs. Functional studies also indicate that both drug families act at PFC level.
CONCLUSION: Atypical antipsychotic drugs likely exert their therapeutic activity by a preferential action on PFC neurons, thus modulating the PFC output to basal ganglia circuits. Classical antipsychotics also interact with these PFC targets in addition to blocking massively striatal D2 receptors.