Kurita
et al. have reported chronic treatment with atypical antipsychotic drugs (
clozapine and
risperidone) decreases expression of metabotropic glutamate 2 receptor (
mGlu2, also known as
Grm2), restrains the therapeutic effects of atypical antipsychotic drugs, and acetylates histone at its promoter gene in the mouse and human frontal cortex. They have also shown that additional treatment with
SAHA as a histone deacetylase (HDAC) inhibitor prevents this decrease in
mGlu2, and augments the behavioral effects of atypical antipsychotics drugs. These data suggest that HDAC2 may be a new therapeutic target to augment the treatment of schizophrenia. (Notice that these products are for research purpose only.)