| pubmed-article:9799403 | pubmed:abstractText | The authors studied effects of opioid receptor agonists on neuronal nicotinic-receptor-mediated current in PC12 cells using whole-cell current recording. At 1 microM, [d-Ala, N-Me, Phe, Gly-ol]- enkephalin (DAMGO), a selective micro receptor agonist, or 10 microM methionine-enkephalin, a micro and delta receptor agonist, did not inhibit the current elicited by 30 microM nicotine significantly. Dynorphin A (1-17) (0.1-1 microM), an endogenous kappa receptor agonist, and U50488 (0.1-10 microM), a non-peptide selective kappa 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 kappa receptor antagonist, or by inclusion of guanosine 5'-O-(2-thiobiphosphate) (GDP[beta-S]), a GTP binding protein blocker, into the pipette solution. These results demonstrate that two kappa 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. | lld:pubmed |
