The neuroprotective actions of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX) in a rat focal ischaemia model
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The neuroprotective action of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX) in a rat focal ischaemia model
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2021, Bioorganic and Medicinal Chemistry LettersThe effect of AMPA receptor blockade on spatial information acquisition, consolidation and expression in juvenile rats
2016, Neurobiology of Learning and MemoryCitation Excerpt :The 5 mg/kg NBQX dose is estimated to produce over 60% inhibition of AMPA-evoked spike activity in hippocampal neurons while the 10 mg/kg dose is estimated to produce over 80% inhibition of AMPA-evoked spike activity (Chizh et al., 1994; Mathiesen, Varming, & Jensen, 1998; Nielsen et al., 1999). The inhibition of in vivo AMPA-evoked spike activity lasts approximately 30–40 min (Gill et al., 1992; Mathiesen et al., 1998). Drug solutions were thawed on the day of use.
Calpains and neuronal damage in the ischemic brain: The swiss knife in synaptic injury
2016, Progress in NeurobiologyCitation Excerpt :In the ischemic brain, the role of AMPAR in excitotoxic injury is primarily (but not exclusively) linked to the depolarization of the membrane which removes the Mg2+ block of nearby NMDAR. Several studies using in vivo and in vitro models of brain ischemia showed neuroprotective effects resulting from inhibition of AMPAR and KAR (Buchan et al., 1991; Gill et al., 1992; Montero et al., 2007; Schielke et al., 1999). The subunit composition of AMPAR expressed in neurons was also found to change in the ischemic brain.
Bioenergetics of cerebral ischemia: A cellular perspective
2008, NeuropharmacologyCitation Excerpt :The extracellular concentration of glutamate increases during both global (Benveniste et al., 1984) and focal ischemia (Hillered et al., 1989; Takagi et al., 1993). As will be described later, excess extracellular glutamate is toxic for both neurons and oligodendrocytes, and glutamate effects on NMDA and AMPA receptors is a major reason for ischemic death of these 2 cell types (Rod and Auer, 1989; Gill et al., 1992; Diemer et al., 1992; Zhang et al., 1997; Giovannelli et al., 2002; Schäbitz et al., 2000; Gressens et al., 2005). During brain ischemia or simulated ischemia in cultured cells or brain slices the increase is initially mainly due to an increased formation and release of glutamate from glutamine in intact glutamatergic neurons (Bosley et al., 1983; Goldberg et al., 1988; Huang and Hertz, 1994, 1995; Huang et al., 1997; Håberg and Sonnewald, 2004), subsequently to reversal of glutamate uptake carriers (Madl and Burgesser, 1993; Rossi et al., 2000; Phillis et al., 2000; Bonde et al., 2003), phospholipase-triggered impairment of membrane integrity (Phillis and O'Regan, 1996), and swelling-induced opening of anion channels (Phillis et al., 1997; Kimelberg and Mongin, 1998), and eventually to activity of extracellular glutaminase released from dead neurons (Newcomb et al., 1997, 1998; Mena et al., 2000).
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