Alteration in the expression of brain-derived neurotrophic factor (BDNF), which has crucial roles in central nervous system neurons, has been proposed to associate with mental disorders including schizophrenia. As many evidences suggest a BDNF downregulation (brain tissue and serum) in patients with schizophrenia, in the present study, we conducted application of phencyclidine (PCP; an NMDA receptor inhibitor), a drug causing schizophrenia-like symptoms, to cultured neurons prepared from rats cerebral cortex, and determined amount of BDNF mRNA. We found that PCP acutely reduced total BDNF mRNA levels. Actinomycin-D (ActD), a transcription inhibitor, also decreased total BDNF mRNA, and co-application with PCP did not demonstrate additional decrease, implying both PCP and ActD influence BDNF mRNA using similar mechanism. When BDNF exons including exon-I, -IV, and -VI were examined, decrease in levels of exon IV-containing transcript was the most evident. Moreover, we found that blockade of CaMKII/CREB similarly decreased mRNA of BDNF in our cultures (Synapse. 2014, Jun;68(6):257-65). This project was supported by Grant-in-Aid for Scientific Research (B) (JSPS KAKENHI Grant Number 24300139) and Challenging Exploratory Research (JSPS KAKENHI Grant Number 25640019) (T. N.) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.