Introduction: Hyperprolactinemia is a common serious side effect of antipsychotic medications that are currently used in the treatment of patients with schizophrenia. Pharmacogenetic approaches offer the possibility of identifying patient-specific biomarkers for predicting the risk of this side effect. We investigated a possible relationship between variants (SNPs) in genes for cytochrome 2D6 (CYP2D6), dopamine-2 receptor (DRD2) and serotonin-2C receptor (HTR2C) and antipsychotic drug-induced hyperprolactinemia in patients with schizophrenia. Methods: Overall, 128 Russian patients with paranoid schizophrenia (61F/67M, aged 18-65 y) were included. Serum prolactin concentration was measured with ELISA. DNA analysis and genotyping of CYP2D6 (rs3892097), DRD2 (rs6275) and HTR2C (rs6318) genes was done with StepOnePlus Real-Time PCR System using TaqMan® SNP Genotyping Assays (Applied Biosystems, USA). Results: Our study showed an association of the CYP2D6 (rs3892097) and HTR2C (rs6318) gene polymorphism with hyperprolactinemia in patients with schizophrenia on the background of therapy. No associations were identified between the DRD2 (rs6275) gene polymorphism and the risk of antipsychotic-induced hyperprolactinemia in patients with schizophrenia. Conclusion: Our study confirms a contribution of genetic factors to the antipsychoticinduced hyperprolactinemia in patients with schizophrenia. Further studies are required to unravel the genetic predictors of antipsychotic-induced side effects and to develop the personalized treatment strategies for patients with schizophrenia.

Background: D2 dopamine receptor gene has been reported to be one of the most relevant candidate genes in schizophrenia. In this study, we investigated the association between TaqIA and TaqIB dopamine D2 receptor polymorphisms and psychopathology of schizophrenia.Methods: The study subjects were 38 acutely exacerbated schizophrenic patients who were all Iranian descent. The control population consisted of 63 healthy individuals with almost the same age as patients and were also of Iranian decent. The TaqIA and TaqIB genotypes, the A1 and A2 alleles, and the B1 and B2 were determined by restriction fragment length polymorphism of the amplified DNA fragments by polymerase chain reaction.Results: For each polymorphism (A or B) the patients were categorized according to their genotype into three groups; i.e. the patients with alleles A1/A1, A1/A2, A2/A2; B1/B1, B1/B2, and B2/B2. No significant association was found between Taq1A or Taq1B gene polymorphisms and schizophrenia in patients compared to the controls. When study subjects were stratified according to their gender, the distribution of the A1/A1 genotype did was significantly different in both men and women (patients vs. controls).Conclusion: Our findings show that there is no genetic association between Taq1A and Taq1B gene polymorphisms and schizophrenia. Further clinical studies should be conducted to confirm and further evaluate these findings.

Background Attention deficit hyperactivity disorder (ADHD) is a multi-factorial disorder that has defined by hyperactivity, impulsivity and attention deficits. Various neurotransmitters such as dopamine can play a role in its pathophysiology. The aim of this study was to examine the association of two common single nucleotide polymorphisms in DRD2 gene, Taq I A (T/C) and Taq I B (G/A), with ADHA risk among Iranian-Azeri population. Materials and Methods A study of case– control association was performed with 89 samples with attention deficit hyperactivity disorder and 96 healthy subjects. Peripheral blood samples were used for Genomic DNA extraction by salting-out method. SNP genotyping was carried out by PCR-RFLP technique. The collected data were analyzed through javastant online statistics software, using Chi-square, with a significance level of 0. 05. Results There was not a significant difference in the allele and genotype frequencies between ADHD and Taq1B polymorphism in cases and controls (P>0. 05). In the Taq IA of DRD2 gene, TT homozygous dominants and CC homozygous recessives were more frequent in case group than in control group but significant difference was not observed (P>0. 05). Also, T/C heterozygotes were more frequent among the control group than the case group, and difference was significant (P<0. 05). Conclusion Our data supports lack of association between Taq1A and Taq1B gene polymorphisms and ADHD.

Background Attention deficit hyperactivity disorder (ADHD), is a multifactorial disorder and converging evidence has implicated abnormalities of dopamine neurotransmission. The aim of this study was to examine the association of-141 polymorphisms in DRD2 gene with ADHA among Iranian-Azeri population. Materials and Methods A case– control association study included 153 patients with attention deficit hyper activity disorder (case group), and 133 healthy subjects (control group). Genomic DNA was extracted peripheral blood samples by salting-out method. Single nucleotide polymorphism (SNP) genotyping was performed by Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The data analysis was performed through Chi-square, with a significance level of 0. 05. Results: There was not significant difference in the allele and genotype frequencies between ADHD and-141C Ins/Del polymorphism in cases and controls (P>0. 05). Ins/Ins homozygous dominants were more frequent in control group than the case group, but there was not significant difference observed (P>0. 05). Del/Del homozygous dominants were not observed. No significant difference was detected in the allele and genotype frequencies between ADHD and-141 Insertion/Deletion polymorphism in cases and control groups (P>0. 05). Conclusion Our results do not detected association between the-141C Ins/Del, rs1799732, polymorphism and ADHD disorder in population of Children in Iranian-Azeri.

Objective(s): Regulation of pro-inflammatory factors such as TNF-𝛼 , which are secreted by the immune cells through induction of their several receptors including dopamine receptors (especially DRD2 and DRD3) is one of the noticeable problems in diabetic severe foot ulcer healing. This study was conducted to evaluate the alteration of TNF-𝛼 in plasma as well as DRD2 and DRD3 changes in PBMCs of diabetics with severe foot ulcers. Materials and Methods: Peripheral blood samples were collected from 31 subjects with ulcers, 29 without ulcers, and 25 healthy individuals. Total mRNA was extracted from PBMCs for the study of DRD2, DRD3, and TNF-𝛼 gene expression variations. Expression patterns of these genes were evaluated by real-time PCR. Consequently, concentration of TNF-𝛼 was investigated in plasma. Results: Significant decrease in gene expression and plasma concentration of TNF-𝛼 in PBMCs was observed in both patient groups at P<0. 05. These diminutions are correlated to the decrease in the expression of both DRD2 and DRD3 in PBMCs of both patient groups. Also, the same relationship is present between expressions of two new DRD3 transcripts with TNF-𝛼 downturn. Conclusion: We concluded that DRD2 and DRD3 expression alteration and presence of new DRD3 transcripts can be effective in reduction of TNF-α expression as a pro-inflammatory factor. Performing complementary studies, may explain that variations in DRD2 and DRD3 are prognostic and effective markers attributed to the development of diabetes severe foot ulcers.

Introduction: Negative early-life experiences (e. g. having an aggressive father) can leave long-lastingimpacts on the behavior. However, it is not clear if they influence learning and memory. Methods: In this study, we investigated the influences that the presence of an aggressive father had on the level of passive avoidance learning and spatial memory. We also studied the changes in the dopamine receptor D2 (DRD2) and peroxisome proliferator-activated receptor gamma coactivator 1-α,(PGC-1α, ) gene expression in the hippocampus. Then, we evaluated if a DRD2 antagonist (sulpiride, 0. 125, 0. 25, or 0. 5 μ, g/rat) could modulate these changes. Results: We found that the subjects exposed to early-life stress made by aggressive fathers had impaired passive avoidance learning and spatial memory compared to subjects with normal fathers. Treatment with sulpiride improved passive avoidance learning and spatial memory in rats with aggressive fathers. The rats with aggressive fathers also had higher expression of the DRD2 gene in their hippocampus than those with normal fathers, while the PGC-1α,gene expression was not different among groups. Treatment with sulpiride (0. 125, 0. 25, or 0. 5 μ, g/ rat) reduced the DRD2 gene expression in those with aggressive fathers to the normal level compared to those with normal fathers. Conclusion: These data suggest that having and living in a shared place with an aggressive father, even without any physical contact, can detrimentally affect passive avoidance learning and spatial memory which is accompanied by the increased expression of the DRD2 gene. Also, sulpiride as a dopaminergic antagonist could reverse this process.