| pubmed-article:18537670 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18537670 | lifeskim:mentions | umls-concept:C0058698 | lld:lifeskim |
| pubmed-article:18537670 | lifeskim:mentions | umls-concept:C0682972 | lld:lifeskim |
| pubmed-article:18537670 | lifeskim:mentions | umls-concept:C0001443 | lld:lifeskim |
| pubmed-article:18537670 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:18537670 | lifeskim:mentions | umls-concept:C1372999 | lld:lifeskim |
| pubmed-article:18537670 | lifeskim:mentions | umls-concept:C1519814 | lld:lifeskim |
| pubmed-article:18537670 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:18537670 | pubmed:dateCreated | 2008-6-9 | lld:pubmed |
| pubmed-article:18537670 | pubmed:abstractText | Adenosine A(2A)-dopamine D(2) receptor interactions play a very important role in striatal function. A(2A)-D(2) receptor interactions provide an example of the capabilities of information processing by just two different G protein-coupled receptors. Thus, there is evidence for the coexistence of two reciprocal antagonistic interactions between A(2A) and D(2) receptors in the same neurons, the GABAergic enkephalinergic neurons. An antagonistic A(2A)-D(2) intramembrane receptor interaction, which depends on A(2A)-D(2) receptor heteromerization and G(q/11)-PLC signaling, modulates neuronal excitability and neurotransmitter release. On the other hand, an antagonistic A(2A)-D(2) receptor interaction at the adenylyl-cyclase level, which depends on G(s/olf)- and G(i/o)-type V adenylyl-cyclase signaling, modulates protein phosphorylation and gene expression. Finally, under conditions of upregulation of an activator of G protein signaling (AGS3), such as during chronic treatment with addictive drugs, a synergistic A(2A)-D(2) receptor interaction can also be demonstrated. AGS3 facilitates a synergistic interaction between G(s/olf) - and G(i/o)-coupled receptors on the activation of types II/IV adenylyl cyclase, leading to a paradoxical increase in protein phosphorylation and gene expression upon co-activation of A(2A) and D(2) receptors. The analysis of A(2)-D(2) receptor interactions will have implications for the pathophysiology and treatment of basal ganglia disorders and drug addiction. | lld:pubmed |
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| pubmed-article:18537670 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18537670 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18537670 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18537670 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18537670 | pubmed:issn | 1873-4286 | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:LluisCC | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:FrancoRR | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:CunhaRR | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:SchiffmannS... | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:PopoliPP | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:FerréSS | lld:pubmed |
| pubmed-article:18537670 | pubmed:author | pubmed-author:WoodsA SAS | lld:pubmed |
