1 copolamine completely blocked the effects of arecoline.

2  and sensitize worms to the toxic effects of arecoline.

3 ol and approximately 30-230 times lower than arecoline.

4 zamine alkaloids is described, starting from arecoline.

5 ubthreshold) could potentiate the effects of arecoline, a cholinergic agonist, or L-glutamate, a glut

6                                Specifically, arecoline, a major betel nut alkaloid, reduced miR329, m

7 le repolarization--when worms are exposed to arecoline, a muscarinic agonist.

8 l agonist iperoxo (IXO), the partial agonist arecoline (ARC), and the inverse agonist 3-quinuclidinyl

9                      Moreover, we identified arecoline hydrobromide (AH) as a covalent ACAT1 inhibito

10 of this class were synthesized starting from arecoline hydrobromide and obtained in optically pure fo

11 ll members of this series were prepared from arecoline hydrobromide in optically pure form and were e

12 d the dose of bicuculline, in the septum, or arecoline in the hippocampus that was needed to improve

13  than before PAR training, blocked the usual arecoline-induced enhancement of response latencies.

14  into the septum, but it reduced the dose of arecoline needed to improve retention in the hippocampus

15 t of increasing the doses of bicuculline and arecoline needed to improve retention.

16 ected into the septum, increased the dose of arecoline needed to improve retention.

17                           The dose of either arecoline or L-glutamate needed to improve retention was

18 omimetic drugs, either a muscarinic agonist (arecoline, pilocarpine or oxotremorine), an acetylcholin

19 ing muscarinic cholinergic receptor agonist, arecoline, resulted in an even more impressive suppressi

20 scopolamine was given to young rats prior to arecoline, the dose-effect curve for enhanced latency ti

21                       We found that 4NQO and arecoline upregulated miR-211 expression in OSCC cells.