PMID- 8478697 OWN - NLM STAT- MEDLINE DCOM- 19930524 LR - 20191101 IS - 0270-6474 (Print) IS - 1529-2401 (Electronic) IS - 0270-6474 (Linking) VI - 13 IP - 5 DP - 1993 May TI - G(olf) and Gs in rat basal ganglia: possible involvement of G(olf) in the coupling of dopamine D1 receptor with adenylyl cyclase. PG - 2237-48 AB - Using specific antibodies and cDNA probes, we have investigated, in rat basal ganglia, the distribution and the regulation of the expression of the alpha subunits of Gs and G(olf), two GTP-binding proteins (G-proteins) that stimulate adenylyl cyclase. We confirmed that G(olf) alpha is highly expressed in caudate-putamen, nucleus accumbens, and olfactory tubercle, whereas Gs alpha is less abundant in these areas than in the other brain regions. Intrastriatal injections of quinolinic acid decreased dramatically the levels of G(olf) alpha protein in the striatum and the substantia nigra, and those of G(olf) alpha mRNA in the striatum. Retrograde lesions of striatonigral neurons with volkensin reduced markedly the levels of D1 dopamine (DA) binding sites, as well as those of G(olf) alpha protein and mRNA in the striatum, without altering D2 binding sites. In contrast, both types of lesions increased the levels of Gs alpha protein in the striatum and substantia nigra. Immunocytochemistry showed the presence of G(olf) alpha protein in striatal medium-sized neurons and in several other neuronal populations. These results demonstrate that striatonigral neurons contain high levels of G(olf) alpha and little, if any, Gs alpha, suggesting that the coupling of D1 receptor to adenylyl cyclase is provided by G(olf) alpha. The levels of G(olf) alpha were five- to sixfold higher in the striatum than in the substantia nigra, indicating a preferential localization of G(olf) alpha in the somatodendritic region of striatonigral neurons and providing a basis for the low efficiency of D1 receptor coupling in the substantia nigra. Six weeks after 6-hydroxydopamine lesions of DA neurons, an increase in G(olf) alpha (+53%) and Gs alpha (+64%) proteins was observed in the striatum. This increase in G(olf) alpha levels may account for the DA-activated adenylyl cyclase supersensitivity, without change in D1 receptors density, that follows destruction of DA neurons. Fine regulation of the levels of G(olf) alpha in physiological or pathological situations may be a critical parameter for the efficiency of DA neurotransmission. FAU - Herve, D AU - Herve D AD - Chaire de Neuropharmacologie, INSERM U 114, College de France, Paris. FAU - Levi-Strauss, M AU - Levi-Strauss M FAU - Marey-Semper, I AU - Marey-Semper I FAU - Verney, C AU - Verney C FAU - Tassin, J P AU - Tassin JP FAU - Glowinski, J AU - Glowinski J FAU - Girault, J A AU - Girault JA LA - eng PT - Comparative Study PT - Journal Article PL - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Glycoproteins) RN - 0 (Plant Lectins) RN - 0 (Plant Proteins) RN - 0 (RNA, Messenger) RN - 0 (Receptors, Dopamine D1) RN - 0 (Ribosome Inactivating Proteins, Type 2) RN - 91933-11-8 (volkensin) RN - EC 3.2.2.- (N-Glycosyl Hydrolases) RN - EC 3.6.1.- (GTP-Binding Proteins) RN - EC 4.6.1.1 (Adenylyl Cyclases) RN - F6F0HK1URN (Quinolinic Acid) RN - VTD58H1Z2X (Dopamine) SB - IM MH - Adenylyl Cyclases/*metabolism MH - Animals MH - Basal Ganglia/*metabolism MH - Brain/metabolism MH - Corpus Striatum/cytology/metabolism MH - Dopamine/physiology MH - GTP-Binding Proteins/*physiology MH - *Glycoproteins MH - Immunohistochemistry MH - Male MH - *N-Glycosyl Hydrolases MH - Neurons/physiology MH - *Plant Lectins MH - Plant Proteins/pharmacology MH - Quinolinic Acid/pharmacology MH - RNA, Messenger/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Receptors, Dopamine D1/*metabolism MH - Ribosome Inactivating Proteins, Type 2 MH - Substantia Nigra/cytology/metabolism MH - Tissue Distribution PMC - PMC6576551 EDAT- 1993/05/01 00:00 MHDA- 1993/05/01 00:01 PMCR- 1993/11/01 CRDT- 1993/05/01 00:00 PHST- 1993/05/01 00:00 [pubmed] PHST- 1993/05/01 00:01 [medline] PHST- 1993/05/01 00:00 [entrez] PHST- 1993/11/01 00:00 [pmc-release] AID - 10.1523/JNEUROSCI.13-05-02237.1993 [doi] PST - ppublish SO - J Neurosci. 1993 May;13(5):2237-48. doi: 10.1523/JNEUROSCI.13-05-02237.1993.