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- Title
δ-, but not µ-, opioid receptor stabilizes K<sup>+</sup> homeostasis by reducing Ca<sup>2+</sup> influx in the cortex during acute hypoxia.
- Authors
Chao, Dongman; Bazzy-Asaad, Alia; Balboni, Gianfranco; Ying Xia
- Abstract
Past work has shown that δ-opioid receptor (DOR) activation by [D-Ala2,D-Leu5]-enkephalin (DADLE) attenuated the disruption of K+ homeostasis induced by hypoxia or oxygen-glucose deprivation (OGD) in the cortex, while naltrindole, a DOR antagonist blocked this effect, suggesting that DOR activity stabilizes K+ homeostasis in the cortex during hypoxic/ischemic stress. However, several important issues remain unclear regarding this new observation, especially the difference between DOR and other opioid receptors in the stabilization of K+ homeostasis and the underlying mechanism. In this study, we asked whether DOR is different from µ-opioid receptors (MOR) in stabilizing K+ homeostasis and which membrane channel(s) is critically involved in the DOR effect. The main findings are that (1) similar to DADLE (10 µM), H-Dmt-Tic-NH-CH (CH2&bond;COOH)-Bid (1–10 µM), a more specific and potent DOR agonist significantly attenuated anoxic K+ derangement in cortical slice; (2) [D-Ala2, N-Me-Phe4, glycinol5]-enkephalin (DAGO; 10 µM), a MOR agonist, did not produce any appreciable change in anoxic disruption of K+ homeostasis; (3) absence of Ca2+ greatly attenuated anoxic K+ derangement; (4) inhibition of Ca2+-activated K+ (BK) channels with paxilline (10 µM) reduced anoxic K+ derangement; (5) DADLE (10 µM) could not further reduce anoxic K+ derangement in the Ca2+-free perfused slices or in the presence of paxilline; and (6) glybenclamide (20 µM), a KATP channel blocker, decreased anoxia-induced K+ derangement, but DADLE (10 µM) could further attenuate anoxic K+ derangement in the glybenclamide-perfused slices. These data suggest that DOR, but not MOR, activation is protective against anoxic K+ derangement in the cortex, at least partially via an inhibition of hypoxia-induced increase in Ca2+ entry-BK channel activity. J. Cell. Physiol. 212: 60–67, 2007. © 2007 Wiley-Liss, Inc.
- Subjects
OPIOID receptors; POTASSIUM; CALCIUM; CEREBRAL anoxia; HYPOXEMIA; HOMEOSTASIS
- Publication
Journal of Cellular Physiology, 2007, Vol 212, Issue 1, p60
- ISSN
0021-9541
- Publication type
Article
- DOI
10.1002/jcp.21000