HDAC2 may be a New Target for Schizophrenia Treatment
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.)
- HDAC2 regulates atypical antipsychotic responses through the modulation of mGlu2 promoter activity
- M. Kurita, T. Holloway, A. García-Bea, A. Kozlenkov, A. K. Friedman, J. L. Moreno, M. Heshmati, S. A. Golden, P. J. Kennedy, N. Takahashi, D. M. Dietz, G. Mocci, A. M. Gabilondo, J. Hanks, A. Umali, L. F. Callado, A. L. Gallitano, R. L. Neve, L. Shen, J. D. Buxbaum, M.-H. Han, E. J. Nestler, J. J. Meana, S. J. Russo, J. González-Maeso, Nat. Neurosci. 2012, 15, 1245.