Lipid-induced modulation of opiate receptors in mouse brain membranes.
The binding of [3H] D-Ala-enkephalinamide (DAEA) to crude mitochondrial fractions (P2M) from mouse forebrain was determined after modulation of membrane lipid microviscosity. Lipid fluidization of P2M membranes, following treatment with egg lecithin, resulted in a 50% loss of specific binding of DAEA. Increasing the P2M lipid microviscosity, by incorporation of cholesteryl hemisuccinate (CHS), increased the accessibility of the opiate receptors up to a peak level of 170% which decreased sharply upon further increase in lipid microviscosity. The processes resulting from lipid rigidification may have important implications for aging and for drug addiction.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D004745:Enkephalins / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects; D008563:Membrane Lipids; D051379:Mice; D010713:Phosphatidylcholines / Q000494:pharmacology; D011957:Receptors, Opioid / Q000378:metabolism*; D014357:Trypsin / Q000494:pharmacology
D004745:Enkephalins; D008563:Membrane Lipids; D010713:Phosphatidylcholines; D011957:Receptors, Opioid; C027970:enkephalin, AlaNH2(5)-; D014357:Trypsin