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. 2019 Feb 7;13:64. doi: 10.3389/fnins.2019.00064

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Copyright © 2019 Khansari and Halliwell.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Involvement of K channels in the neuroprotective effects of MFA in vitro: hippocampal neurons in culture for 9 days were exposed to glutamate (5 μM). Drugs were co-incubated during glutamate exposure and immediately after for 24 h. Cell death was quantified using the Cytotox-96 24 h later. Treatment with MFA (100 μM) or nicorandil (NIC, 100 μM) reduced glutamate mediated cell death by 65 and 60% (^∗∗p ≤ 0.01) respectively. Tetraethylammonium (TEA, 30 mM) alone did not significantly alter the level of glutamate induced cell death. Co-application of TEA (30 mM) completely abolished the neuroprotective effect of nicorandil (100 μM) but co-incubation of TEA (30 mM) with MFA (100 μM) did not significantly affect the neuroprotective actions of this fenamate NSAID.