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manner. Therefore, gene polymorphisms of dopaminergic components, such as dopamine receptor D2 ( DRD2 ), dopamine receptor D3 ( DRD3 ) and dopamine β-hydroxylase ( DβH ) that regulate dopamine neurotransmission or metabolism could influence the predisposition of an individual to alcohol dependence. DRD2 is one of the most widely studied genes of the dopaminergic pathway in relation to addictive behaviors. The DRD2 rs1800497 (32806 C>T or TaqIA) gene polymorphism has been suggested to affect DRD2 availability. The TaqI A1 allele was associated with reduced number

. Arch Gen Psychiatry 1991, 48(8): 757-759. [4] Clarke TK, Weiss AR, Ferarro TN, Kampman KM, Dackis CA, Pettinati HM, O’Brien CP, Oslin DW, Lohoff FW, Berrettini WH: The dopamine receptor D2 (DRD2) SNP rs1076560 is associated with opioid addiction. Ann Hum Genet 2014, 78(1): 33-39. [5] David SP, Strong DR, Munafò MR, Brown RA, Lloyd-Richardson EE, Wileyto PE, Evins EA, Shields PG, Lerman C, Niaura R: Bupropion efficacy for smoking cessation is influenced by the DRD2 Taq1A polymorphism: analysis of pooled data from two clinical trials. Nicotine Tob Res 2007, 9

modulation of A 2a gene expression on normal aging and in pathological conditions as AD are still unclear, but the use of non-selective antagonists like caffeine to treat AD-related cognitive deficits is showing promising results [18, 21, 22]. In our present work, we tested the effect of caffeine on the mRNA expression of a package of confirmed AD-involved genes in two concentrations, 10 and 100 μM, and analyzed the correlation of two major transmitter systems in the cell communications systems, adenosine (A 2aa , A 2ab , and A 2b ) and dopamine (drd 2a and drd 2c

revealing risk factors of ineffectiveness before treatment begins [ 7 ]. The highest level of evidence is shown for the CYP2D6 gene’s polymorphisms [ 7 ]. There is also evidence of the significance of polymorphisms of the type 2 dopamine receptor gene (DRD2) [ 8 ] and type 1A serotonin receptor gene [ 9 ]. It is worth noting that the gene ABCB1 encoding the transport protein P-glycoprotein (P-gp) is also an important candidate gene. P-gp is involved in the efflux transport of xenobiotics, preventing the ingestion of drugs through cell membranes. ABCB1 polymorphisms can

schizophrenia. Pharmacogenomics J. 2011 Feb; 11(1): 35-44. 65. Nyberg S, Eriksson B, Oxenstierna G, Halldin C, and Farde L. Suggested minimal effective dose of risperidone based on PET measured D2 and 5-HT2A receptor occupancy in schizophrenic patients. Am J Psychiatry. 1999; 156: 869-75. 66. 4-25 25. Zai CC, et al. Meta-analysis of two dopamine D2 receptor gene polymorphisms with tardive dyskinesia in schizophrenia patients. Mol Psychiatry. 2007; 12: 794. 67. Lencz T, Robinson DG, Napolitano B, et al. DRD2 promoter region variation predicts antipsychoticinduced weight gain

Abstract

The dopaminergic system is of crucial importance for understanding human behavior and the pathogenesis of many psychiatric and neurological conditions. The majority of studies addressing the localization of dopamine receptors (DR) examined the expression of DR in neurons, while its expression, precise anatomical localization and possible function in glial cells have been largely neglected. Here we examined the expression of D2-like family of DR in neuronal and glial cells in the normal human brain using immunocytochemistry and immunofluorescence. Tissue samples from the right orbitomedial (Brodmann’s areas 11/12), dorsolateral (areas 9/46) and dorsal medial (area 9) prefrontal cortex were taken during autopsy from six subjects with no history of neurological or psychiatric disorders, formalin-fixed, and embedded in paraffin. The sections were stained using novel anti-DRD2, anti-DRD3, and anti-DRD4 monoclonal antibodies. Adjacent sections were labeled with an anti-GFAP (astroglial marker) and an anti-CD68 antibody (macrophage/microglial marker). The pyramidal and non-pyramidal cells of all three regions analyzed had strong expression of DRD2 and DRD4, whereas DRD3 were very weakly expressed. DRD2 were more strongly expressed in layer III compared to layer V pyramidal neurons. In contrast, DRD4 receptors had a stronger expression in layer V neurons. The most conspicuous finding was the strong expression of DRD2, but not DRD3 or DRD4, receptors in the white matter fibrous astrocytes and in layer I protoplasmic astrocytes. Weak DRD2-immunoreactivity was also observed in protoplasmic astrocytes in layers III and V. These results suggest that DR-expressing astrocytes directly participate in dopaminergic transmission of the human prefrontal cortex.

Medical School, Florence, Italy; 3 Department of Neurosurgery, Kopfklinikum, W-8520 Erlangen, Germany; 4 Department of Medical Genetics, Groningen University, Groningen, Holland; 5 Department of Pharmacology, Federal University of Minas Gerais, Belo-Horizonte, Brazil ABSTRACT The molecular mechanisms underlying pitu- itary tumor development are largely unknown, but presumably involve inactivation of the MENl gene, and in prolactinomas, uncoupling of the dopamine receptor (DRD2) from intra- cellular effectors. To test this notion, 50 sporadic pituitary tumors (28

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, Alain Eschalier, Jérôme Busserolles, Beata Sperlagh and Adrián Llerena Pharmacogenetics in pain treatment 131 Original Articles Georgia Ragia, Ivan Veresies, Louiza Veresie, Kyriakos Veresies and Vangelis G. Manolopoulos Association study of DRD2 A2/A1, DRD3 Ser9Gly, DbH −1021C > T, OPRM1 A118G and GRIK1 rs2832407C > A polymorphisms with alcohol dependence 143 Athira Bindu Murali, Belsy Boban, Aswathy Karoor Shanmughan, Karthikeyan Marimuthu, Aravind Ramakrishnan Sreelatha and Augustine Xavier Medication therapy management (MTM): an innovative approach to

father as the donor. Millennium Health received an oral swab sample from the patient for its polymerase chain reaction (PCR)-based pharmacogenetics test (14 genes: CYP2B6 (*1, *4, *6, *9, *18), CYP2C9 (*1, *2, *3, *5, *8, *11), CYP2C19 (*1, *2, *3, *4, *8, *17), CYP2D6 (*1, *2, *2A, *3, *4, *4N, *5, *6, *9, *10, *17, *29, *35, *36, *41, allele-specific gene duplication), CYP3A4 (*1, *22), CYP3A5 (*1, *3), DRD2 (rs1799732 Ins/Del), HLA-B*15:02 , HTR2C (rs3813929C/T), VKORC1 (rs9923231A/G), COMT (rs4680A/G), OPRM1 (rs1799971A/G), MTHFR (rs1801131

genotyping of OB (mutation C)T Arg)Trp in codon 105), PPAR-g2 (mutation C)A Pro)Gln in codon 115), UCP1 (polymorphism A)G in the promoter region –3826), b2AR (polymorphism C)G Gln)Glu in codon 27), b3AR (polymorphism T)G Trp)Arg in codon 64), DRD2 (polymorphism C)T in the non-coding sequence 39), LPL-H (polymorphism T)G in intron 8), LPL-P (C)T in intron 6), TNF-a (polymorphism G)A in the promoter region –308), PPAR-g (polymorphism A)G in codon 12 (Pro12)Ala)) and apoCIII (polymorphism C3238)G) were performed using the restriction fragment length polymorphism method (RFLP