Epigenetic regulation of G protein coupled receptor signaling and its implications in psychiatric disorders. (August 2016)

• Record Type: Journal Article
• Authors: Dogra, Shalini; Sona, Chandan; Kumar, Ajeet; Yadav, Prem N.
• Is Part Of: International journal of biochemistry & cell biology. Volume 77:Part B(2016:Aug.)
• Page Start: 226
• Page End: 239
• Publication Date: 2016-08
• Subjects: GPCRs Gprotein-coupled receptors -- HDAC histone deacetylase -- CNS central nervous system -- GWAS genome-wide association studies -- GEFs guanine nucleotide exchange factors -- GDP guanosine diphosphate -- GTP guanosine triphosphate -- WHO world health organization -- CRF corticotrophin releasing factor -- OXT oxytocine -- MDD major depressive disorder -- LSD1 lysine-specific histone demethylase 1 -- SVZ subventricular zone -- CRHR corticotropin-releasing hormone receptor -- 5-HT 5-hydroxytryptamine -- BDNF brain-derived neurotrophic factor -- SSRIs selective serotonin reuptake inhibitors -- PFC prefrontal cortex -- mGluR metabotropic glutamate receptors -- HPA hypothalamus pituitary axis -- CORT corticosterone -- GR glucocorticoid receptor -- SIRT sirtuin -- 5-HTTLPR serotonin transporter linked polymorphic region -- 5-HTT serotonin transporter -- PVN para ventricular nucleus -- CREB cAMP response element-binding protein -- CBP CREB-binding protein -- BNST bed nucleus of the stria terminalis -- Dnmt DNA methyltransferase -- NAc nucleus accumbens -- GIH gestational intermittent hypoxia -- αCGRP calcitonin gene-related peptide -- FRL flinders resistant line -- AVP arginine vasopressin -- OXTR oxytocin receptor -- MT melatonin receptors -- VTA ventral tegmental area -- DA dopamine -- DRD dopamine receptors -- MSNs medium spiny neurons -- THC tetrahydrocannabinol -- OPRM1 μ receptor gene -- CPP conditioned place preference -- NGF nerve growth factor -- SH-SY5Y human neuroblastoma cell line -- NK neurokinin -- ERK extracellular signal-regulated kinase -- CB1R cannabinoid receptor-1 -- ATP adenosine triphosphate -- NMDAR N-methyl-d-aspartate receptor -- DRG Dorsal root ganglia -- Calca calcitonin-Related Polypeptide Alpha -- Trpv1 Transient receptor potential cation channel subfamily V member 1 -- SAHA Suberanilohydroxamic acid -- TSA Trichostatin A -- ET-1 endothelin-1 -- ETA receptor : endothelin A receptor -- ETB receptor endothelin B receptor -- NRSF neuron-restrictive silencer factor -- REST RE1-silencing transcription factor -- CXCL CXC chemokine ligand -- CXCR CXC chemokine receptor -- mGluRs metabotropic glutamate receptors -- GABA Gamma-Aminobutyric acid -- GABABR gamma-aminobutyric acid −B receptor -- CFA complete freund's adjuvant -- GAD65 Glutamate decarboxylase 65 -- GAD1 glutamate decarboxylase 1; Epigenetic -- HDAC -- Histone methylation -- Histone acetylation -- DNA methylation -- GPCR -- CRH -- CRHR1 -- Oxytocin -- mGluR2 -- Endothelin receptors -- CGRP -- Opioids -- Amygdala -- VTA -- DRG -- GAD65 -- Depression -- Addiction -- Neuropathic pain; Biochemistry -- Periodicals; Cytology -- Periodicals; Biochemistry -- Periodicals; Cell Biology -- Periodicals; Biochimie -- Périodiques; Cytologie -- Périodiques; Biochimie; Cytologie; Biochemistry; Cytology; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); Periodicals; 572.05
• DOI: 10.1016/j.biocel.2016.03.012
• Languages: English
• ISSNs: 1357-2725

Abstract

Abstract: G protein-coupled receptors (GPCRs) act as a relay center through which extracellular signals, in the form of neurotransmitters or therapeutics, are converted into an intracellular response, which ultimately shapes the overall response at the tissue and behavioral level. Remarkably in similar ways, epigenetic mechanisms also modulate the expression pattern of a large number of genes in response to the dynamic environment inside and outside of the body, and consequently overall response. Emerging evidences from the pharmacogenomics and preclinical studies clearly suggest that these two distinct mechanisms criss-cross each other in several neurological disorders. At one hand such cross-talks between two distinct mechanisms make disease etiology more challenging to understand, while on the other hand if dealt appropriately, such situations might provide an opportunity to find novel druggable target and strategy for the treatment of complex diseases. In this review article, we have summarized and highlighted the main findings that tie epigenetic mechanisms to GPCR mediated signaling in the pathophysiology of central nervous system (CNS) disorders, including depression, addiction and pain.