Introduction: Schizophrenia is a psychosis considered multifactorial, involving genetic and external
factors. Dopamine receptors (D1-D5) are central to the understanding of dopaminergic theory. The
distribution of these receptors in various brain areas and their excitatory or inhibitory action on the
synthesis of cAMP correlates brain areas where there is underactive and dopaminergic hyperactivity
associated with schizophrenia. D1 receptors are excitatory and its reduction in the prefrontal cortex is
possibly associated with deficit cognitive. No agreement on the pattern of cognitive impairment, but the
precocity of these changes and their long-term stabilization is well documented. Objectives: address some
gaps dopaminergic theory: the unsatisfactory results of antipsychotics on negative symptoms and
antipsychotics; the relationship dopamine-receptors in the frontal lobes and changes in cognition.
Method: Researching data in Medline/PubMed and Lilacs utilizing the terms: schizophrenia, dopamine
theory, cognition schizophrenia, antipsychotics, dopamine receptors, cognition deficit in schizophrenia.
Discussion: the dopaminergic theory has been the most widely accepted, pointing to the brain of the
neurotransmitter dopamine dysregulation and its receptores.Uma hypofunction dopamine in the
prefrontal cortex would be responsible for negative symptoms, deficit cognitive and a primary event in
schizophrenia , leading to a hyperfunction dopaminergic secondary in the striatum, which would be the
cause of positive symptoms. As cognitive changes have higt prevalence, are present even in the
premorbid. Studies “ post mortem” phase are facing considerable reduction of D1 receptors in the
prefrontal cortex of schizophrenic patients cognitive deficit. Conclusion: It is believed that atypical
antipsychotics do not cause extrapyramidal symptoms because they have a connection to the D2 receptor
less strongly than the D2-dopamine, so there is no shortage in the extrapyramidal system which would be
the cause of Parkinsonian syndrome with the use of typical antipsychotics . A hypothesis for the
unsatisfactory results of antipsychotics in negative symptoms and cognitive deficit is the excitatory action
of D1 receptors in the prefrontal cortex.A dopaminergic hypofunction cortex in this area has been
correlated with negative symptoms and cognitive deficit. An ideal antipsychotic should, in additionto
inhibit the mesolimbic pathway, leverage the mesocortical pathway, which supplies the prefrontal cortex,
this may be possible through difrenças between D1 and D2 receptors.

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