ISSN:
1432-2013
Keywords:
Key words Dynorphins
;
Kappa opioid receptor
;
Nicotinic receptors
;
Opioids
;
Patch clamp
;
PC12 cells
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract The authors studied effects of opioid receptor agonists on neuronal nicotinic-receptor-mediated current in PC12 cells using whole-cell current recording. At 1 µM, [d-Ala, N-Me, Phe, Gly-ol]- enkephalin (DAMGO), a selective µ receptor agonist, or 10 µM methionine-enkephalin, a µ and δ receptor agonist, did not inhibit the current elicited by 30 µM nicotine significantly. Dynorphin A (1–17) (0.1–1 µM), an endogenous κ receptor agonist, and U50488 (0.1–10 µM), a non-peptide selective κ receptor agonist, depressed the nicotine-induced current reversibly in a dose-dependent manner. They accelerated the current decay, resulting in greater effects on the non-desensitized current than the peak current. These effects were not affected by nor-binaltrophimine, a selective κ receptor antagonist, or by inclusion of guanosine 5′-O-(2-thiobiphosphate) (GDP[β-S]), a GTP binding protein blocker, into the pipette solution. These results demonstrate that two κ opioid receptor agonists, dynorphin A (1–17) and U50488, inhibit neuronal nicotinic-receptor-mediated current without the involvement of opioid receptors or GTP binding proteins. The acceleration of the current decay suggests a direct action on nicotinic receptors such as open channel block, or augmentation of desensitization. Modulation of neuronal nicotinic receptors by dynorphins may play a role in some areas where dynorphin release sites and neuronal nicotinic receptors are colocalized.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004240050719
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