Hugonin Loïc, Vukojević Vladana, Bakalkin Georgy, Gräslund Astrid
Department of Biochemistry and Biophysics, Arrhenius Laboratories, Stockholm University, S-10691 Stockholm, Sweden.
FEBS Lett. 2006 May 29;580(13):3201-5. doi: 10.1016/j.febslet.2006.04.078. Epub 2006 May 4.
Dynorphins, endogeneous opioid peptides, function as ligands to the opioid kappa receptors and induce non-opioid excitotoxic effects. Here we show that big dynorphin and dynorphin A, but not dynorphin B, cause leakage effects in large unilamellar phospholipid vesicles (LUVs). The effects parallel the previously studied potency of dynorphins to translocate through biological membranes. Calcein leakage caused by dynorphin A from LUVs with varying POPG/POPC molar ratios was promoted by higher phospholipid headgroup charges, suggesting that electrostatic interactions are important for the effects. A possibility that dynorphins generate non-opioid excitatory effects by inducing perturbations in the lipid bilayer of the plasma membrane is discussed.
强啡肽作为内源性阿片肽，充当阿片κ受体的配体并诱导非阿片类兴奋毒性作用。我们在此表明，大强啡肽和强啡肽A而非强啡肽B，会在大单层磷脂囊泡（LUVs）中引起渗漏效应。这些效应与先前研究的强啡肽透过生物膜的能力相当。强啡肽A导致不同POPG/POPC摩尔比的LUVs中钙黄绿素渗漏，较高的磷脂头部基团电荷会促进这种渗漏，这表明静电相互作用对这些效应很重要。本文讨论了强啡肽通过诱导质膜脂质双层扰动产生非阿片类兴奋效应的可能性。
