کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2200676 | 1099960 | 2013 | 6 صفحه PDF | دانلود رایگان |

We have comparatively investigated the effects of Hardwickiic acid and Salvinorin A on the K+-evoked overflow of [3H]noradrenaline ([3H]NA) and [3H]dopamine ([3H]DA) from mouse hippocampal and striatal nerve terminals, respectively. The K+-evoked overflow of [3H]DA was inhibited in presence of Salvinorin A (100 nM) but not in presence of Hardwickiic acid (100 nM). Hardwickiic acid (100 nM) mimicked Salvinorin A (100 nM) in facilitating K+-evoked hippocampal [3H]NA overflow and the two compounds were almost equipotent. Facilitation of [3H]NA overflow caused by 100 nM Hardwickiic acid was prevented by the κ-opioid receptor (KOR) antagonist norbinaltorphimine (norBNI, 100 nM) and by the selective δ-opioid receptor (DOR) antagonist naltrindole (100 nM), but was not altered by 100 nM D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP), a selective μ-opioid receptor (MOR) antagonist. We conclude that Hardwickiic acid modulates hippocampal [3H]NA overflow evoked by a mild depolarizing stimulus by acting at presynaptic opioid receptor subtypes.
Journal: Neurochemistry International - Volume 62, Issue 4, March 2013, Pages 354–359