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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

In vivo effects of the I(2)-alkylating agent BU99006 on the immunodensity of imidazoline receptor proteins in the mouse brain.

The binding sites for imidazol(ine)/guanidine drugs (identified inter alia with [(3)H]-clonidine and [(3)H]-idazoxan) are heterogeneous in nature, and various pharmacologic types of imidazoline receptors (IRs) have been characterized (I(1)R, I(2A)R, I(2B)R, and I(3)R). IR-receptor proteins have also been immunodetected using an antibody raised against an approximately 70-kD idazoxan/clonidine binding protein, which probably recognizes all types of IRs. In this study, the in vivo effects of the selective I(2)-alkylating agent BU99006 (5-isothiocyanato-2-benzofuranyl-2-imidazoline) on immunoreactive IR proteins were assessed in the mouse brain to unravel the molecular nature of the I(2)R subtypes. In mouse tissues (cerebral cortex, liver, testis, and kidney) this antibody revealed the presence of 30-, 43-, 45-, 66-, and/or 85-kD IR proteins. Treatment with BU99006 (20 mg/kg, intraperitoneally, for 4 hours) significantly decreased the immunodensity of specific IR proteins in the brain (30 kD: 249%; 45 kD: 237%; 66 kD: 218%). In contrast, the immunoreactivities of 43-kD and 85-kD IR proteins were not altered after I(2)R alkylation. Prolonged treatment with BU99006 (20 mg/kg, intraperitoneally. for 8 hours) resulted in modest but significant increases in the expression of all the immunodetected IR proteins in the mouse brain (20%-36%), suggesting compensatory increases in IR protein synthesis after alkylation of I(2) sites. The results indicate that the 30-kD and 45-kD proteins, but not the 43-kD and 85-kD proteins, immunodetected in the mouse brain are related to the I(2)R.[1]


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