Allen Institute for Artificial Intelligence
supp.ai logo
supp.ai

Discover Supplement-Drug Interactions

Disclaimer: The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The tool is not a substitute for the care provided… (more)
Last Updated: 2 years ago

Possible Interaction: Gamma-Aminobutyric Acid and Nicotine

Research Papers that Mention the Interaction

In vitro exposure of cells to single doses or seven days of nicotine induced the protein expression of MMP-2, MMP-9 and EGR-1 and these responses were blocked by GABA.
BMC Cancer  •  2014  |  View Paper
Both in vivo and in vitro the administration of nicotine stimulated an overflow of aspartate, glutamate and GABA.
PloS one  •  2012  |  View Paper
Interestingly, GABA , being an antagonist to cAMP signaling, showed a promising intervention by reversing the stimulatory effect of nicotine on cancer growth and all signaling pathways.
Current cancer drug targets  •  2012  |  View Paper
However, other neurochemical systems also participate in the addictive effects of nicotine including glutamate, cannabinoids, GABA and opioids.
Neuroscience & Biobehavioral Reviews  •  2010  |  View Paper
Accordingly, pharmacological agents that target brain acetylcholine, DA, glutamate, GABA , or endocannabonoid signaling systems have been proposed to interrupt nicotine action.
Acta Pharmacologica Sinica  •  2009  |  View Paper
Nicotine additionally reduced the protein levels of both GAD isozymes and GABA in tumor tissue.
Treatment with GABA abolished these responses to nicotine and blocked the development of xenografts in mice not exposed to nicotine.
Carcinogenesis  •  2009  |  View Paper
Our data suggest that nicotine increases the SHH-mediated malignant potential of PCSCs and that GABA prevents these effects.
European journal of cancer  •  2016  |  View Paper
Nicotine treatment also down-regulated expression of the GABA synthesizing enzyme GAD 65 and the level of endogenous GABA, while treatment of NSCLC cells with GABA inhibited cell proliferation.
PloS one  •  2012  |  View Paper
All of the observed adverse effects of chronic nicotine were reversed by treatment of the cells with γ-aminobutyric acid , suggesting the potential usefulness of this agent for the improvement of PDAC intervention strategies in smokers.
Carcinogenesis  •  2012  |  View Paper
Second, we discuss preclinical evidence that suggests nicotine affects GABA neuronal function indirectly by a primary action at neuronal nicotinic acetylcholine receptors.
Neuropharmacology  •  2011  |  View Paper
Show More