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

Binding of [3H]2-(2-benzofuranyl)-2-imidazoline (BFI) to human brain: potentiation by tranylcypromine.

Recently, a new imidazoline (I2) ligand, [3H]2-(2-benzofuranyl)-2-imidazoline (BFI) was shown to be more selective for I2 vs alpha 2 binding in rodent brain. We characterized [3H]BFI binding in human brain cortex and lateral reticular nucleus ( NRL). Membranes were incubated with [3H]BFI at 22 degrees C in 50 mM Tris, 1.5 mM EDTA at pH 7. 5. Saturation experiments with [3H]BFI (0.5-80 nM) were analyzed using non-linear curve fitting. The NRL had 4X more binding sites than cortex with similar affinity (Bmax = 2085 +/- 732 and 471 +/- 41 fmol/mg protein; KD = 9.3 +/- 3.5 and 11.9 +/- 2.7 nM, respectively). In competition studies, cortical [3H]BFI binding was displaced in order of decreasing potency by clorgyline > BFI > or = cirazoline > idazoxan > or = guanabenz > clonidine > RX821002. The monoamine oxidase (MAO) inhibitor tranylcypromine (TCP) (1 nM-10 microM), markedly enhanced [3H]BFI binding in both NRL and cortex. Enhanced binding was maximal at 300 nM (12 X control) and returned to baseline at 30 microM. Potentiation was not seen with pargyline or clorgyline. TCP did not effect [3H]BFI binding in rat cortex, or [3H]idazoxan binding in human cortex and NRL. In human cortex, inhibition of MAO by preincubation with pargyline (10 micro M) abolished the TCP effect. Upon preincubation with TCP, the stimulation of [3H]BFI binding was dose-dependently related to a simultaneous inhibition of MAO. Thus, [3H]BFI labels a site in human NRL and cortex that appears similar to the previously described I2 site labeled by [3H]idazoxan. However, [3H]BFI binding is dramatically stimulated by TCP in human brain via a mechanism dependent on endogenous MAO activity.[1]

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