Alcohol hangover induces nitric oxide metabolism changes by impairing NMDA receptor-PSD95-nNOS pathway

dc.contributor.author Karadayian, Analía G.
dc.contributor.author Bustamante, Juanita
dc.contributor.author Lores-Arnaiz, Silvia
dc.date.accessioned 2023-10-17T21:44:55Z
dc.date.available 2023-10-17T21:44:55Z
dc.date.issued 2021-5-5
dc.description.abstract Alcohol hangover is defined as the combination of mental and physical symptoms experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration approaches zero. We previously evidenced increments in free radical generation and an imbalance in antioxidant defences in non-synaptic mitochondria and synaptosomes during hangover. It is widely known that acute alcohol exposure induces changes in nitric oxide (NO) production and blocks the binding of glutamate to NMDAR in central nervous system. Our aim was to evaluate the residual effect of acute ethanol exposure (hangover) on NO metabolism and the role of NMDA receptor-PSD95-nNOS pathway in non-synaptic mitochondria and synaptosomes from mouse brain cortex. Results obtained for the synaptosomes fraction showed a 37% decrease in NO total content, a 36% decrease in NOS activity and a 19% decrease in nNOS protein expression. The in vitro addition of glutamate to synaptosomes produced a concentration-dependent enhancement of NO production which was significantly lower in samples from hangover mice than in controls for all the glutamate concentrations tested. A similar patter of response was observed for nNOS activity being decreased both in basal conditions and after glutamate addition. In addition, synaptosomes exhibited a 64% and 15% reduction in NMDA receptor subunit GluN2B and PSD-95 protein expression, respectively. Together with this, glutamate-induced calcium entry was significant decreased in synaptosomes from alcohol-treated mice. On the other hand, in non-synaptic mitochondria, no significant differences were observed in NO content, NOS activity or nNOS protein expression. The expression of iNOS remained unaltered in synaptosomes and non-synaptic mitochondria. Here we demonstrated that hangover effects on NO metabolism are strongly evidenced in synaptosomes probably due to a disruption in NMDAR/PSD- 95/nNOS pathway.
dc.identifier.citation Karadayian, A.G.; Bustamante, J.; Lores-Arnaiz, S. (2021). Alcohol hangover induces nitric oxide metabolism changes by impairing NMDA receptor-PSD95-nNOS pathway. In: Nitric Oxide 113-114:29-49
dc.identifier.other 10.1016/j.niox.2021.04.009
dc.identifier.uri https://repositorio.uai.edu.ar/handle/123456789/1891
dc.language.iso en
dc.publisher Elsevier
dc.subject alcohol hangover
dc.subject nitric oxide
dc.subject nitric oxide synthase
dc.subject GluN2B
dc.subject PSD-95
dc.subject synaptosomes
dc.title Alcohol hangover induces nitric oxide metabolism changes by impairing NMDA receptor-PSD95-nNOS pathway
dc.type ARTICULO
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