Abstract:
:G protein-coupled receptor 35 (GPR35) is an orphan G protein-coupled receptor (GPCR) that can be activated by kynurenic acid at high micromolar concentrations. A previously unappreciated mechanism of action of GPR35 has emerged as a Gαi/o-coupled inhibitor of synaptic transmission, a finding that has significant implications for the accepted role of kynurenic acid as a broad-spectrum antagonist of the NMDA, AMPA/kainite and α7 nicotinic receptors. In conjunction with previous findings that link agonism of GPR35 with significant reduction in nociceptive pain, GPR35 has emerged as a potential effector of regulation of mechanical sensitivity and analgesia of the Ret tyrosine kinase, and as a receptor involved in the transmission of anti-inflammatory effects of aspirin- potentially through affecting leucocyte rolling, adhesion and extravasation. Single nucleotide polymorphisms of GPR35 have linked this receptor to coronary artery calcification, inflammatory bowel disease and primary sclerosing cholangitis, while chromosomal aberrations of the 2q37.3 locus and altered copy number of GPR35 have been linked with autism, Albight's hereditary osteodystrophy-like syndrome, and congenital malformations, respectively. Herein, we present an update on both the pharmacology and potential function of GPR35, particularly pertaining to the nervous system. This review forms part of a special edition focussing on the role of lipid-sensing GPCRs in the nervous system. This article is part of the Special Issue entitled 'Lipid Sensing G Protein-Coupled Receptors in the CNS'.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Mackenzie AE,Milligan Gdoi
10.1016/j.neuropharm.2015.07.035subject
Has Abstractpub_date
2017-02-01 00:00:00pages
661-671issue
Pt Beissn
0028-3908issn
1873-7064pii
S0028-3908(15)30042-3journal_volume
113pub_type
杂志文章,评审abstract::Although depression is a severe and life-threatening psychiatric illness, its pathogenesis still is essentially unknown. Recent studies highlighted the influence of environmental stress factors on an individual's genetic predisposition to develop mood disorders. In the present study, we employed a well-validated stres...
journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章,评审
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
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doi:10.1016/0028-3908(95)00108-i
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章,评审
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更新日期:2015-07-01 00:00:00
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journal_title:Neuropharmacology
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pub_type: 杂志文章
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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abstract::Nicotinic acetylcholine receptors (nAChRs) are highly conserved between humans and non-human primates. Conservation exists at the level of genomic structure, protein structure and epigenetics. Overall homology of nAChRs at the protein level is 98% in macaques versus 89% in mice, which is highly relevant for evaluating...
journal_title:Neuropharmacology
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