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Table 2

Summary of effects of antagonists on D-Asp whole-cell currents. Effect on L-Glu currents designated with italics

AntagonistTarget receptorPercentage of block (−) or potentiation (+)N
SITS (100 μM)Cl channels−1 ± 17%7
TBOA (1 mM)EAATs−10 ± 10%*8
Kynurenate (1 mM)Nonselective L-GluRs−27 ± 19%*9
L-Glu:65 ± 13%*8
Role of NMDARs
APV (100 μM)NMDARs+100 ± 88%*7
−22 ± 16%*15
L-Glu:0.8±10%8
PPDA (50 μM)NMDARs—selective for NR2C/NR2D−46 ± 22%*19
L-Glu: −46±11%*8
Kyn + APV + PPDA (1 mM + 100 μM + 50 μM)All L-GluRs−69 ± 15%*9
L-Glu: −76±21%*9
TCS46b (50 μM)NMDARs—selective for NR1A/NR2B−16 ± 16%*7
MK-801 (500 nM)NMDARs−13 ± 36%14
Memantine (100 μM)NMDARs−6 ± 9%6
Role of non-NMDARs
CNQX (100 μM)AMPA/kainate Rs+30 ± 18%*8
NBQX (5 μM)AMPA/kainate Rs+15 ± 14%*7
DNQX (100 μM)Kainate Rs−22 ± 37%8
UBP302 (50 μM)Kainate Rs+10 ± 23%6
CTZ (200 μM)AMPAR desensitization+3 ± 20%7
*Significantly different from control recorded in absence of antagonist via paired t-test at P≤ 0.05.