| Autor: |
Akunne, Hyacinth, Monn, J., Thurkauf, Andrew, Jacobson, Arthur, Rice, Kenner, Linders, Joannes, Jiang, Q., Porreca, F., Rothman, Richard |
| Zdroj: |
Neurochemical Research; Apr1994, Vol. 19 Issue 4, p385-389, 5p |
| Abstrakt: |
The electrophilic affinity ligand, (+)-3-isothiocyanato-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine hydrochloride {(+)-MK801-NCS} was characterized for its ability to acylate phencyclidine (PCP) and sigma binding sites in vivo. Initial studies, conducted with mouse brain membranes, characterized the binding sites labeled by [H]1-[1-(2-thienyl)cyclohexyl]piperidine ([H]TCP). The Kd values of [H]TCP for PCP site 1 (MK801-sensitive) and PCP site 2 (MK801-insensitive) were 12 nM and 68 nM, with Bmax values of 1442 and 734 fmol/mg protein, respectively. Mice were sacrificed 18-24 hours following intracerebroventricular administration of the acylator. The administration of (+)-MK801-NCS increased [H]TCP binding to site 2, but not to site. 1. Although (+)-MK801-NCS decreased [H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d; cbcyclohepten-5,10-imine maleate ([H](+)-MK801) binding to site 1, it had no effect on [H]TCP binding to site 1. Viewed collectively with other published data, these data support the hypothesis that PCP sites 1 and 2 are distinct binding sites, and that [H]TCP and [H](+)-MK801 label different domains of the PCP binding site associated with the NMDA receptor. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Full text from SpringerLink