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Last Updated: 3 months ago

Possible Interaction: Ethanol and Mecamylamine

supplement:

Ethanol

Research Papers that Mention the Interaction

Even when the lower BALs were taken into account, mecamylamine reduced ratings of stimulation after alcohol ( Addiction Research Center Inventory A scale).
Alcoholism, clinical and experimental research  •  2005  |  View Paper
In laboratory animals, mecamylamine , a central nicotinic receptor antagonist, reduces the consumption of and preference for alcohol.
It was hypothesized that mecamylamine (7.5 and 15 mg) would attenuate the stimulant-like subjective effects of alcohol (0.8 g/kg) and decrease the self-reported desire to consume additional alcohol beverages.
RESULTS Me amylamine at tenuated the stimulant and euphoric effects of alc ohol an d reduced the self-reported desire to consume additional alcohol beverages.
Alcoholism, clinical and experimental research  •  2003  |  View Paper
This study was conducted to test the hypothesis that, during the ascending limb of the blood alcohol concentration curve, mecamylamine would reduce the stimulating and pleasurable effects of an intoxicating dose of alcohol in humans.
Alcoholism, clinical and experimental research  •  2002  |  View Paper
Rat CT responses to ethanol are also partially inhibited by nAChR blockers, mecamylamine and dihydro-β-erythroidine.
PloS one  •  2018  |  View Paper
The nAChR modulators: mecamylamine , dihydro-β-erythroidine, and CP-601932 (a partial agonist of the α3β4* nAChR), inhibited CT responses to nicotine, ethanol , and acetylcholine.
PloS one  •  2015  |  View Paper
Pre-treatment with mecamylamine inhibited the rate-inhibiting properties of ethanol in the VTA, but not in the nAc.
Alcohol  •  2014  |  View Paper
Coinfusion with 200 μM mecamylamine (nACh antagonist) or 100 and 200 μM zacopride (5-HT3 receptor antagonist) blocked the observed nicotine enhancement of EtOH seeking.
Psychopharmacology  •  2014  |  View Paper
For both rat strains, blood alcohol concentration in the mecamylamine pretreatment group was significantly less at this time interval by about 50-60 mg/dL, suggesting a mechanism whereby mecamylamine can mitigate some of the acute effects of alcohol (e.g., on VC components N39 and P46).
However, mecamylamine pretreatment reduced the effects of alcohol on components N39 and P46.
On separate days, either saline or mecamylamine was given 10 min prior to either saline or ethanol.
Progress in Neuro-Psychopharmacology and Biological Psychiatry  •  2013  |  View Paper
In addition, chronic administration of mecamylamine into ethanol diet-fed mice markedly attenuated the ethanol withdrawal sign scores, thus supporting the contention that nAChR is involved in ethanol dependence.
In conclusion, our results suggest that mecamylamine exhibited inhibitory effects on ethanol withdrawal signs which could be mediated through nAChR.
Results showed that acute administration of mecamylamine (1–4 mg/kg, intraperitoneally) dose-dependently attenuated ethanol withdrawal-induced signs, and these effects were comparable with those of diazepam (1–2 mg/kg, intraperitoneally).
Behavioural pharmacology  •  2010  |  View Paper
However, intra-CA1 or -BLA microinjection of mecamylamine (1-4 microg/rat) reversed the response induced by the microinjection of nicotine (1 microg/rat, intra-CA1 or -BLA) plus ethanol (0.5 g/kg i.p.)
Moreover, intra-CA1 administration of nicotine plus ethanol increased the locomotor activity on the test day which was reversed by pretreatment with mecamylamine , while other treatments had no effect on locomotor activity.
Neuroscience  •  2010  |  View Paper
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