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Synaptic transmission and excitability during hypoxia with inflammation and reoxygenation in hippocampal CA1 neurons

Title
Synaptic transmission and excitability during hypoxia with inflammation and reoxygenation in hippocampal CA1 neurons
Authors
Yang, Yoon-SilSon, Sook JinChoi, Joon HoRah, Jong-Cheol
Issue Date
2018-08
Citation
Neuropharmacology, 138, 20-31
Type
Article
Article Type
Article
Keywords
HypoxiaInflammationReoxygenationSynaptic transmissionHyperexcitabilityHyperpolarization-activated cation current (Ih)
ISSN
0028-3908
Abstract
Although a number of experimental and clinical studies have shown that hypoxia typically accompanies acute inflammatory responses, the combinatorial effect of the two insults on basic neural function has not been thoroughly investigated. Previous studies have predominantly suggested that hypoxia reduces network activity; however, several studies suggest the opposite effect. Of note, inflammation is known to increase neural activity. In the current study, we examined the effects of limited oxygen in combination with an inflammatory stimulus, as well as the effects of reoxygenation, on synaptic transmission and excitability. We observed a significant reduction of both synaptic transmission and excitability when hypoxia and inflammation occurred in combination, whereas reoxygenation caused hyperexcitability of neurons. Further, we found that the observed reduction in synaptic transmission was due to compromised presynaptic release efficiency based on an adenosine-receptor–dependent increase in synaptic facilitation. Excitability changes in both directions were attributable to dynamic regulation of the hyperpolarization-activated cation current (Ih) and to changes in the input resistance and the voltage difference between resting membrane potential and action potential threshold. We found that zatebradine, an Ih current inhibitor, reduced the fluctuation in excitability, suggesting that it may have potential as a drug to ameliorate reperfusion brain injury. © 2018 Elsevier Ltd
URI
http://hdl.handle.net/20.500.11750/6583
DOI
10.1016/j.neuropharm.2018.05.011
Publisher
Elsevier Ltd
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