Regular ArticleExcitotoxic Cell Death Dependent on Inhibitory Receptor Activation
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2019, iScienceCitation Excerpt :The central component of our model is an excitatory storm and the attendant positive feedback loop involving ion channels and neurotransmitters (Figure 2C). Thus, it predicts that interrupting this loop (inducing neuroprotection) by targeting specific dopamine machinery (Vaarmann et al., 2013; Cepeda et al., 1998; Odaka et al., 2014), chloride channels (Hasbani et al., 1998; Rungta et al., 2015; Takeuchi et al., 2011; Chen et al., 1999), or L-type calcium channels (Szydlowska and Tymianski, 2010; Mark et al., 2001; Hasbani et al., 1998), should prevent degeneration. To test these predictions, we exposed worms to a combination of BaCl2 and one of several blockers (previously characterized in planaria or other invertebrates), tracking the incidence of degeneration over 3 days and comparing with BaCl2-only controls.
GABA<inf>A</inf> receptor chloride channels are involved in the neuroprotective role of GABA following oxygen and glucose deprivation in the rat cerebral cortex but not in the hippocampus
2013, Brain ResearchCitation Excerpt :A number of studies that support this hypothesis have shown protective effects of chloride-free media in both organotypic cultures and brain slices (Takahashi et al., 1999; Grondahl et al., 1998). The beneficial or detrimental effects of the ischaemia-induced chloride fluxes, through ligand-operated chloride channels, such as GABAA receptors, have been discussed at length (see Erdö et al., 1991; Hasbani et al., 1998; Inglefield and Schwartz-Bloom, 1998; Chen et al., 1999; Galeffi et al., 2004; Babot et al., 2005; Kumar et al., 2006). And, GABA-mediated neuroprotection, following OGD in rabbit cortical slices, has been previously described for a range of concentrations between 30 and 1000 μM (Ricci et al., 2011).
An immunological basis of hyperphagia driven by GABAergic dysfunction in Prader-Willi Syndrome
2012, Medical HypothesesEffects of inhibitory amino acids on expression of GABA <inf>A</inf> Rα and glycine Rα1 in hypoxic rat cortical neurons during development
2011, Brain ResearchCitation Excerpt :At present, most of the information is obtained from homomeric GlyRα1 (Lynch, 2004). GABAA and glycine receptors play an important role in the neuronal responses to environmental stress (Chen et al., 1999; Zhao et al., 2005). Hypoxic/ischemic stress causes excessive accumulation of excitatory amino acids, which initiate the process of neuronal injury via neurotoxicity (Banasiak et al., 2000).
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