Effect of hypoxia and glucose deprivation on ATP level, adenylate energy charge and [Ca2+]0-dependent and independent release of [3H]dopamine in rat striatal slices
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Hypoxia post-conditioning promoted glycolysis in mice cerebral ischemic model
2020, Brain ResearchCitation Excerpt :Reduced delivery of glucose and oxygen during brain ischemia can cause energy failure through adenosine triphosphate (ATP) depletion. ATP production in the ischemic area is decreased or even abolished which subsequently initiates cell death (Milusheva et al., 1996; Robbins and Swanson, 2014). Glucose can support glycolytic ATP production even in the absence of oxygen, and increased glycolysis in the ischemic brain is known to improve cell survival (Sims and Muyderman, 2010).
Cerebral ischemia/repefusion injury: From bench space to bedside
2017, Brain Research BulletinCitation Excerpt :ATP production is decreased or even stopped in response to ischemia, which perturbs the function of the ATP dependent membrane pumps. ( Milusheva et al., 1996) The complete arrest of ATP production leads to cell swelling, disruption of membranes and cell death. The toxic levels of glutamate released from the neurons and glia cells act on NMDA and AMPA channels and increase their permeability to Ca2+.
Lithium and valproate act on the GSK-3β signaling pathway to reverse manic-like behavior in an animal model of mania induced by ouabain
2017, NeuropharmacologyCitation Excerpt :In addition, previous studies also showed that ouabain significantly increases the levels of DA in the striatum and cortical slices from rat brains (Boireau et al., 1998; Obata, 2006; Diniz et al., 2007; Silva et al., 2007). These studies suggest that synaptosomal inhibition of Na+K+ ATPase by ouabain increases intracellular Na+ and thereby is able to induce DA release from the cytoplasm through reverse transport of DAT (Milusheva et al., 1996; Leviel, 2001). Therefore, the increase in DA induced by ouabain may induce the changes in the GSK-3β pathway observed in the present study.
Correlation between the increased release of catecholamines evoked by local anesthetics and their analgesic and adverse effects: Role of K<sup>+</sup> channel inhibition
2016, Brain Research BulletinCitation Excerpt :Subsequently, fractions were collected every 3 min. The radioactivity remaining in the tissue was measured after perfusion (Milusheva et al., 1996), and we calculated the amount (neuronal uptake) of radioactivity at the beginning of the experiments (the sum of radioactivity released during 19 collection periods and the radioactivity remaining after perfusion). In the cerebral cortex samples, 75.2 ± 5.7% (the mean ± SEM of 30 observations) of the total radioactivity was accounted for DA, and 85.6 ± 4.1% (n = 18) was attributed to NA, as measured by high-pressure liquid chromatography combined with scintillation spectrometry.