|1.||Wong, Chih-Shung: 8 articles (05/2013 - 06/2002)|
|2.||Wen, Zhi-Hong: 7 articles (12/2013 - 03/2002)|
|3.||Wen, Z-H: 5 articles (11/2015 - 06/2007)|
|4.||Jean, Y-H: 5 articles (11/2015 - 06/2007)|
|5.||Saransaari, Pirjo: 5 articles (01/2013 - 09/2003)|
|6.||Chang, Yi-Chen: 5 articles (05/2006 - 06/2002)|
|7.||Oja, Simo S: 4 articles (01/2013 - 08/2004)|
|8.||Kimelberg, Harold K: 4 articles (04/2008 - 01/2004)|
|9.||Massieu, L: 4 articles (11/2006 - 10/2000)|
|10.||Hulsebosch, C E: 4 articles (11/2001 - 09/2000)|
03/01/2005 - "This methodology provides the possibility of evaluating the protection against the outflow of excitatory amino acids and against an acute motor disturbance, i.e.contralateral turning to the ischemic side in the first hours after ischemia in awake rats. "
01/06/1992 - "GM1 ganglioside reduces ischemia-induced excitatory amino acid output: a microdialysis study in the gerbil hippocampus."
10/01/1991 - "Although considerable evidence supports a role for excitatory amino acids in the pathogenesis of ischemic neuronal injury, few in vivo studies have examined the effect of increasing durations of ischemia on the extracellular concentrations of these agents. "
01/15/2012 - "At 7 days post-ischemia, expression of excitatory amino acid carrier 1 decreased in the hippocampal CA1 region and cortex, and was accompanied by apoptosis. "
03/01/2008 - "Treatment with RWPC completely prevented the burst of excitatory amino acids that occurred in response to ischemia in untreated rats and significantly reduced brain infarct volumes. "
|2.||Brain Ischemia (Cerebral Ischemia)
09/01/1991 - "Monosialoganglioside GM1 prevents excitatory amino acid (EAA)-related neuronal death in cultured central nervous system (CNS) neurons and reduces the severity of acute brain damage in different experimental models of cerebral ischemia. "
10/19/2001 - "This study suggested that altered brain energy metabolites and excitatory amino acids occurred during cerebral ischemia and and HBO regulated these striatal metabolites, which might contribute to the protective effect of HBO in cerebral ischemia."
04/01/1996 - "To study the changes of excitatory amino acid (EAA) in patients with cerebral ischemia. "
09/01/1995 - "Recently, studies have demonstrated in vitro, that D-2 agonist, at the level of striatum and retina, may represent a powerful signal to inhibit release of excitatory amino acids implicated in cerebral ischemia. "
08/15/1994 - "Since ischemia brain damage is ascribed to an elevated level of extracellular excitatory amino acids (EAAs), this study was undertaken to investigate the effect of GCs on EAA homeostasis in hippocampal cell cultures during the insult of cyanide exposure. "
07/01/2006 - "Excitatory amino acid release and electrocortical brain activity after hypoxemia in near-term lambs."
05/01/2004 - "Activation of ionotropic excitatory amino acid (EAA) receptors in pre-Bötzinger complex (pre-BötC) not only influences the eupneic pattern of phrenic motor output but also modifies hypoxia-induced gasping in vivo by increasing gasp frequency. "
08/01/2000 - "Taken together, these data suggest that EtOH enhances DA release in vivo during short-term hypoxia, possibly through mechanisms other than excitatory amino acid pathways."
01/01/1997 - "A novel in vitro cell culture model has been developed to investigate the mechanisms of delayed neuronal cell death following exposure to excitatory amino acids and hypoxia. "
07/01/1996 - "The cytotoxic effects of hypoxia and excitatory amino acids on cultured retinal ganglion cells were studied. "
|4.||Brain Injuries (Brain Injury)
01/01/2004 - "To assess systematically the efficacy of excitatory amino acid inhibitors on improving patient outcome following traumatic brain injury. "
01/01/2004 - "Trials were included if they were randomised, double-blind, controlled trials where excitatory amino acid inhibitors were administered to patients with traumatic brain injury, within 24 hours of sustaining that injury, and compared to a control group. "
03/01/2001 - "The aim of this study is to monitor excitatory amino acids (EAAs) in the extracellular fluids of the brain and to characterize regional neuronal damage in a new experimental model for brain injury, in which rabbits were exposed to 180-260 krad/s2 rotational head acceleration. "
01/01/1998 - "In previous studies, Katayama and our group have documented a massive increase in excitatory amino acid release following traumatic brain injury, in both rat fluid percussion, and humans [2,5]. "
01/01/1992 - "Recent studies suggest that excitatory amino acids (EAAs) may be important for the development of hypoxic-ischemic brain injury in the newborn. "
06/01/1995 - "In spite of growing evidence for the involvement of the glutamatergic system in mammal's locomotion, studies on behavioral effects induced by the systemic administration of excitatory amino acids not associated to convulsions are lacking. "
07/01/1994 - "Experimental study of the mechanism of seizure induction: changes in the concentrations of excitatory amino acids in the epileptic focus of the cat amygdaloid kindling model."
09/01/1992 - "These neurochemical findings were discussed in relation to previous studies of age-related alterations in excitatory amino acids (EAAs) and the role of EAA and NE in modulating limbic seizures. "
08/20/2015 - "An increase in the release of excitatory amino acids has consistently been observed in the hippocampus during seizures, both in humans and animals. "
09/01/2014 - "AE did not prevent QA-induced seizures; however, it prevented cellular death and disruption of excitatory amino acid transport. "
|1.||Glutamic Acid (Glutamate)
|4.||Excitatory Amino Acids
|5.||Excitatory Amino Acid Antagonists
|6.||AMPA Receptors (AMPA Receptor)
|7.||Valproic Acid (Valproate, Semisodium)
|8.||Aspartic Acid (Aspartate)
|9.||Nitric Oxide (Nitrogen Monoxide)
|10.||Neurotransmitter Agents (Neurotransmitter)