To probe the role of NCX in the AWS pathophysiology, we used SN-6 (2-[[4-[(4-nitrophenyl)methoxy]phenyl]methyl]-4-thiazoli dinecarboxylic acid ethyl ester, R&D Systems, Minneapolis, MN, USA) and KB-R7943 (2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl] isothioureamethanesulfonate, R&D Systems). SN-6 preferentially blocks NCX1rev activity, while KB-7943 inhibits NCX3rev more potently than its forward mode [40 (link)–42 (link)]. SN-6 and KB-R7943 were dissolved in dimethyl sulfonic acid (0.1%) and phosphate-buffered saline (pH 7.4) using sonication (80 kHz, 100% power). The solutions containing SN-6 or KB-R7943 were filtered before focal microinjections within the IC at 5 μg/hemisphere; this dose was chosen based on our published reports [24 (link),43 (link)].
Protocol detail
Probing NCX Role in AWS Pathophysiology
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Corresponding Organization :
Other organizations : Howard University, Georgetown University Medical Center
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Variable analysis
independent variables
- SN-6 (2-[[4-[(4-nitrophenyl)methoxy]phenyl]methyl]-4-thiazoli dinecarboxylic acid ethyl ester)
- KB-R7943 (2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl] isothioureamethanesulfonate)
- Not explicitly mentioned
- Dimethyl sulfonic acid (0.1%)
- Phosphate-buffered saline (pH 7.4)
- Dose of SN-6 and KB-R7943 (5 μg/hemisphere)
- Positive control: Not mentioned
- Negative control: Not mentioned
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