Abstract. Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a clinically aggressive tumor, which frequently presents as cutaneous lesions and subsequently progresses to bone marrow (BM) involvement and leukemic dissemination. BPDCN is a rare entity that belongs in the same class as acute myeloid leukemia-associated precursor neoplasms,

The purpose of the present study was to investigate effects of N-methyl-D-aspartate (NMDA) on proliferation and apoptosis of hippocampal neural stem cells (NSCs) treated with dizocilpine (MK-801). Cultures of hippocampal NSCs were randomly divided into four groups consisting of an untreated control, cells treated with MK-801, NMDA and a combination of MK801 and NMDA (M+N). Proliferative and apoptotic responses for each of the experimental groups were determined by MTS and flow cytometry. The results revealed that MK-801 and NMDA exerted significant effects on hippocampal NSCs proliferation. Cell survival rates decreased in MK-801, NMDA and M+N treated groups compared with the control group. Cells survival rates in NMDA and M+N treated groups increased compared with the MK-801 treated group. MK-801 and NMDA were demonstrated to significantly affect apoptosis in hippocampal NSCs. Total and early stages of apoptosis in MK-801 and NMDA groups significantly increased compared with the control group. Total and early apoptosis of NSCs in the M+N group significantly decreased compared with MK-801 and NMDA groups. Late apoptosis of NSCs in MK-801 and NMDA groups significantly decreased compared with the control group. Late apoptosis of NSCs in the M+N group significantly increased compared with MK-801 and NMDA groups. The present study revealed that MK-801 inhibited proliferation and increased apoptosis in hippocampal NSCs. NMDA may reduce the neurotoxicity induced by MK-801, which may be associated with its activity towards NMDA receptors and may describe a novel therapeutic target for the treatment of schizophrenia.

The aim of the present study was to investigate the characteristics of N‑methyl‑D‑aspartate receptor R1 (NR1) expression and apoptosis in the nerve cells of the hippocampus in schizophrenia‑like mice. C57BL/6 mice were randomly allocated to the following groups: i) Blank group; ii) MK‑801 group; iii) MK‑801+NMDA group, according to body weight. The NMDAR antagonist, MK‑801 (0.6 mg/kg/d) was intraperitoneally injected daily for 14 days to induce a schizophrenia‑like phenotype mouse model, and the effect of the NMDA injection via the lateral ventricle was observed. The results demonstrated that the number of NR1 positive cells in the MK‑801 group increased in the CA1 and DG regions, indicating that NMDA may reverse this change. The level of damage decreased in the MK‑801 treated group when compared with the blank group in the CA3 region. The protein expression of NR1 increased however, at the mRNA expression level, NR1 was lower in the MK‑801 treated group when compared to the blank group; NMDA also reversed this change. In addition, early and total apoptosis detected in the hippocampal nerve cells was significantly increased in the MK‑801 group when compared with the blank group, which was reversible following treatment with NMDA. These results indicated that NMDA may regulate the expression of NR1 and suppress apoptosis in hippocampal nerve cells in schizophrenia‑like mice. Thus, NR1 may be a promising therapeutic target for the treatment of schizophrenia.