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EnglishChronic treatment of mice with the specific gamma-aminobutyrie acid(B) (GABA(B)) receptor antagonist (2S)(+)-5.5-(dimethyl-2-morpholineacetic acid (SCH 50,911) increased both the number of GABA(B) receptors in the whole brain (measured as [H-1]CGP 54626 [S-(R,R)]-3-[[1-(3,4-dichlorophenyl)amino]-2-hydroxypropyl](cyclohexylmethyl)phosphinic acid hydrochloride binding) and the ability of bacloten to activate GABA(B) receptor coupled G-protein (measured as % reduction of the EC50 of baclofen to activate [S-15]GTP gamma S binding). The results indicate that persistent blockade of GABA(B) receptors leads to their compensatory up-regulation and suggest that GABA(B) receptors are tonically activated by endogenous GABA. (c) 2005 Elsevier B.V. All rights reserved.
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| Titolo: | Up-regulation of GABA(B) receptors by chronic administration of the GABA(B) receptor antagonist SCH 50,911 |
| Autori: | |
| Data di pubblicazione: | 2005 |
| Rivista: | |
| Abstract: | Chronic treatment of mice with the specific gamma-aminobutyrie acid(B) (GABA(B)) receptor antagonist (2S)(+)-5.5-(dimethyl-2-morpholineacetic acid (SCH 50,911) increased both the number of GABA(B) receptors in the whole brain (measured as [H-1]CGP 54626 [S-(R,R)]-3-[[1-(3,4-dichlorophenyl)amino]-2-hydroxypropyl](cyclohexylmethyl)phosphinic acid hydrochloride binding) and the ability of bacloten to activate GABA(B) receptor coupled G-protein (measured as % reduction of the EC50 of baclofen to activate [S-15]GTP gamma S binding). The results indicate that persistent blockade of GABA(B) receptors leads to their compensatory up-regulation and suggest that GABA(B) receptors are tonically activated by endogenous GABA. (c) 2005 Elsevier B.V. All rights reserved. |
| Handle: | http://hdl.handle.net/11584/23099 |
| Tipologia: | 1.1 Articolo in rivista |
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