Fig. 5
Elvitegravir does not affect NMDA receptor function in HEK293 cells. Automated patch clamp recordings were performed using the Sophion Qube platform to generate antagonistic dose-response curves of Elvitegravir and NMDA receptor antagonists, D-APV, Ifenprodil, and TCN-201 for human GluN1/GluN2A a or GluN1/GluN2B b NMDA receptors expressed in HEK293 cell lines. Responses to NMDA and glycine (see methods section) were recorded at −70 mV in Mg2+-free extracellular solutions and normalized to responses of the same cells recorded in the absence of Elvitegravir or antagonists. GluN1/GluN2A was blocked by the non-selective NMDA receptor antagonist, D-APV (IC50: 1.477 μM) and the selective GluN2A blocker, TCN-201 (IC50: 0.722 μM) but not the GluN2B antagonist, Ifenprodil (IC50 > 10 μM) or Elvitegravir (IC50 > 300 μM). GluN1/GluN2B was blocked by the non-selective NMDA receptor antagonist, D-APV (IC50: 1.141 μM) and the selective GluN2B blocker, Ifenprodil (IC50: 0.811 μM) but not the GluN2A antagonist, TCN-201 (IC50 > 10 μM) or Elvitegravir (IC50 > 300 μM). Data are shown as individual cell values and a logistic fit of the Hill equation to the data from which IC50 values were estimated. N = 2–8 cells from two independent experiments