Ethanol inhibition of NMDA mediated depolarizations is increased in the presence of Mg2+
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Glutamate Signaling in Alcohol Abuse and Dependence
2014, Neurobiology of Alcohol DependenceInhibition of rat recombinant GluN1/GluN2A and GluN1/GluN2B NMDA receptors by ethanol at concentrations based on the US/UK drink-drive limit
2009, European Journal of PharmacologyGlutamatergic substrates of drug addiction and alcoholism
2008, Biochemical PharmacologyCitation Excerpt :As a result, ethanol inhibits the induction of several forms of neural plasticity such as LTP in the hippocampus [528–531], dorsal striatum [532] (but also see [509]) and bed nucleus of the stria terminalis [533] while enhancing LTD in the hippocampus [534]. The ability of ethanol to inhibit NMDA receptor function is dependent on various factors including the NR1 splice variant that is co-assembled with NR2 subunits [535], extracellular Mg2+ and glycine concentrations [536–540], intracellular Ca2+ concentrations [541], and NMDA receptor phosphorylation by proteins kinases such as Fyn [542–544], PKA [545] but see [546], and PKC [547] as well as by the phosphorylation regulator DAARP-32 [548]. As a result of the ability of ethanol to inhibit NMDA receptor function, NMDA antagonists such as MK-801 can potentiate the effects of acute ethanol such as the duration of ethanol-induced loss-of-righting reflex [549–552] and stimulation of locomotor activity [553–555].
NMDA receptors in alcoholism
2003, International Review of NeurobiologyGlutamate-mediated transmission, alcohol, and alcoholism
2000, Neurochemistry International