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Last Updated: 3 years ago

Possible Interaction: Gamma-Aminobutyric Acid and Nitric Oxide

Research Papers that Mention the Interaction

Endogenous NO modulates the release of acetylcholine, glutamate, aspartate, GABA , serotonin, histamine in distinct brain areas.
Current medicinal chemistry  •  2016  |  View Paper
This action seems to employ an indirect mechanism by which NO may modulate the release of GABA.
Folia histochemica et cytobiologica  •  2006  |  View Paper
In particular, NO heavily influences the excitatory neurotransmitter glutamate, mainly through NMDA receptors, and the inhibitory neurotransmitter GABA , mainly through GABA A receptors.
In vivo  •  2004  |  View Paper
Collectively, these results suggest that short repeated oral administration of GABA has an anxiolytic-like effect possibly via preventing NO reduction caused by stress and improving availability of NO in the frontal cortex.
Psychiatry Research  •  2019  |  View Paper
Nitric oxide NO ) production has correlation with GABA and regulates GnRH secretion.
Ecotoxicology and environmental safety  •  2019  |  View Paper
Ex vivo NO modified GABA-T activity and GABA levels biphasically.
In vitro NO diminished GABA-T activity and increased GABA.
Acta pharmaceutica  •  2018  |  View Paper
Together, these results suggest that NO promotes GABA release by activating TRPC5 channels in AC dendrites.
Journal of neurophysiology  •  2018  |  View Paper
NO subsequently acts presynaptically to enhance GABA release through a soluble guanylate cyclase-mediated pathway.
The Journal of Neuroscience  •  2015  |  View Paper
Further pharmacological experiments, such as the application of a nitric oxide-sensitive guanylyl cyclase (NO-sGC) receptor antagonist, a NOS inhibitor, and NO donors, suggested that NO released from postsynaptic cells mediated FSI and likely activated presynaptic receptors to inhibit GABA release.
The Journal of Neuroscience  •  2014  |  View Paper
Conclusions Our results indicate that NO induces release of aspartate, glutamate, glycine and GABA in cortical neurons and that this release is inhibited by ODQ, an inhibitor of soluble guanylate cyclase.
PloS one  •  2014  |  View Paper
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