Abstract
Quantitative binding studies resolved two high-affinity [3H][D-Ala2,D- Leu5]enkephalin binding sites in rat brain membranes depleted of μ binding sites by pretreatment with the irreversible agent BIT. - The two binding sites had lower (δ(nc-x), Ki = 96.6 nM) and higher ({dncx-1) , Ki = 1.55 nM) affinity for DPDPE. The ligand-selectivity profile of the δ(ncx-1) site was that of a classic δ binding site. The ligand-selectivity profile of the δ(ncx-2) site was neither μ- or δ-like. The Ki values of selected agents for the δ(ncx-2) site were: [pCl]DPDPE (3.9 nM), DPLPE (140 nM), and DAMGO (2.6 nM), under these assay conditions, [3H][D-Ala2,D-Leu5]enkephalin binding to the cells expressing the cloned μ receptor is very low and pretreatment of cell membranes with BIT almost completely inhibits [3H]DAMGO and [3H][D-Ala2,D-Leu5]enkephalin binding. Intracerebroventricular administration of antisense DNA to the cloned delta receptor selectively decreased [3H][D-Ala2,D-Leu5]enkephalin binding to the δ(ncx-1) site. Administration of buprenorphine to rats 24 h prior to preparation of membranes differentially affected μ, δ(ncx-1), and δ(ncx-2) binding sites. Viewed collectively, these studies have identified a novel non-μ- non-δ- like binding site in rat brain.
Original language | English (US) |
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Pages (from-to) | 1079-1090 |
Number of pages | 12 |
Journal | Peptides |
Volume | 19 |
Issue number | 6 |
DOIs | |
State | Published - Jun 1998 |
Keywords
- Acetalin
- Antisense DNA
- Delta receptors
- Ligand binding
- Opiate receptors
ASJC Scopus subject areas
- Biochemistry
- Physiology
- Endocrinology
- Cellular and Molecular Neuroscience