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. Author manuscript; available in PMC: 2021 Aug 15.
Published in final edited form as: Neuropharmacology. 2020 Jan 25;173:107971. doi: 10.1016/j.neuropharm.2020.107971

Table 2.

Effects of PTC-174 and (+)-CIQ on agonist potencies at NMDA receptor subtypes.

glutamate EC50 (μM) nH n glycine EC50 (μM) nH n
GluN1/2C control 0.52 ± 0.05 1.3 6 0.24 ± 0.03 1.6 6
+ 10 μM PTC-174 0.19 ± 0.02* 1.8 6 0.05 ± 0.00* 1.4 6
GluN1/2D control 0.30 ± 0.01 1.7 6 0.12 ± 0.01 1.5 6
+ 10 μM PTC-174 0.11 ± 0.01* 1.5 6 0.03 ± 0.01* 1.2 5
GluN1/2D control 0.21 ± 0.02 1.5 6 0.16 ± 0.01 1.8 8
+ 10 μM (+)-CIQ 0.23 ± 0.01 1.2 6 0.15 ± 0.02 1.2 6

Recombinant GluN1/2C and GluN1/2D NMDA receptor subtypes were expressed in Xenopus oocytes and concentration-response data for glutamate and glycine were measured using two-electrode voltage-clamp electrophysiology. Glutamate EC50 values were generated by activating the receptors with increasing concentrations of glutamate in the continuous presence of 50 μM glycine in the absence and presence of 10 μM PTC-174 or 10 μM (+)-CIQ. Glycine EC50 values were generated by activating the receptors with increasing concentrations of glycine in the continuous presence of 100 μM glutamate in the absence and presence of 10 μM PTC-174 or 10 μM (+)-CIQ. Data are presented as mean ± SEM, nH is the Hill slope, and n is the number of oocytes used to generate the data. Statistical tests were performed using logEC50 values and

*

indicates significantly different from control on the same receptor for the same agonist (P < 0.05; unpaired t-test).