Inhibition of adenosine kinase during oxygen-glucose deprivation in rat cortical neuronal cultures
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Cited by (49)
Adenosine Receptor Biology in the Central Nervous System
2017, Adenosine Receptors in Neurodegenerative DiseasesHuman endothelial progenitor cells rescue cortical neurons from oxygen-glucose deprivation induced death
2016, Neuroscience LettersCitation Excerpt :Nevertheless, we preferred to avoid the use of neuron surrogates such as immortalized neurons, which might have a less sensitive apoptosis and cell death mechanism, that would further limit the results of possible OGD treatment assays. Most studies are limited to the first hours or maximum to the first 24 hrs [1,2,25,32,35]. Considering all the above limits, we observed a certain advantage for neurons provided by indirect co-culture with both endothelial precursor cells and mesenchymal stem cells after OGD in terms of survival.
Adenosine A1 receptor agonist, N6-cyclohexyladenosine, protects myelin and induces remyelination in an experimental model of rat optic chiasm demyelination; Electrophysiological and histopathological studies
2013, Journal of the Neurological SciencesCitation Excerpt :The role of NSCs in myelin repair has been frequently confirmed in previous reports [11–15]. Higher level of adenosine inside the CNS insults is supposed to be the consequence of its increased release and reduced removal and seems to be protective against neural damage [16–18]. On the other hand, several studies have reported the potential role of adenosine A1 receptors in CNS repair.
Astrocytic adenosine kinase regulates basal synaptic adenosine levels and seizure activity but not activity-dependent adenosine release in the hippocampus
2009, NeuropharmacologyCitation Excerpt :For example, shortly after kainic acid treatment there is a transient downregulation of ADK levels, which may exert a protective, anticonvulsant role (Gouder et al., 2004). In addition, hypoxia/ischemia is known to cause inhibition (Decking et al., 1997; Lynch et al., 1998; Kobayashi et al., 2000) and downregulation of ADK (Pignataro et al., 2008) which may contribute, at least in part, to the rapid increase in extracellular adenosine seen under these conditions (Frenguelli et al., 2003, 2007; Pearson et al., 2006), whilst ADP-induced aggregation of ADK exerts another level of control (Sen et al., 2006). Thus, the dynamic regulation of ADK expression and activity is likely to have an important bearing on the availability and role of extracellular adenosine.