There was no significant difference in current amplitude of D-Asp currents in the presence of SITS (Table 2). Table 2 Summary of effects of antagonists on D-Asp whole-cell currents. Effect on L-Glu currents designated with italics Figure 2 Antagonists of D-Asp currents at −30 mV. (A) Whole-cell currents in response to pressure application of D-Asp (1 mM) in ASW (control)
and in ASW plus 1 mM kynurenate (KYN). Inset: whole-cell currents in L-Glu (1 mM) in ASW (control) and in ASW … Figure 5 Effects of bath-applied D-Asp and L-Glu on agonist-evoked currents. (A) Summary of effects of 0.5 mM bath-applied D-Asp (exposure) on L-Glu-activated currents (1 mM). *denotes significant difference from control and washout at P < 0.05 (Student's Inhibitors,research,lifescience,medical ... TBOA (1 mM), a blocker of excitatory amino acid transporters (EAATs), significantly reduced D-Asp currents to a small degree (Fig. 2B; mean decrease 10 ± 10%; P≤ 0.05). D-Asp Inhibitors,research,lifescience,medical currents were significantly reduced in amplitude by 27 ±
19% in the presence of kynurenate (1 mM), a general L-Glu receptor antagonist while L-Glu currents in the same cells were uniformly, significantly reduced to a larger extent at 65 ± 13% block (Fig. 2A and Table 2; P≤ 0.01, Student’s paired t-test). Block of both Ibrutinib clinical trial receptors was reversible. The NMDAR antagonist APV (100 μM) had mixed effects, causing a significant, reversible increase in D-Asp current amplitude Inhibitors,research,lifescience,medical in 7 of 22 cells examined (Fig. 3A; mean increase of 100 ± 88%; P Inhibitors,research,lifescience,medical < 0.05), and a significant, reversible decrease
in all other cells tested (Fig. 3B; mean block of 22 ± 16%; P≤ 0.05). There was no significant difference in D-Asp current amplitude in APV compared to controls when all 22 cells exposed to APV were considered as a single sample. L-Glu currents in the same cells were uniformly unaffected by APV (Fig. 3B, inset; Table 2). PPDA (50 μM), an NMDAR antagonist showing greater preference for vertebrate NR2C and NR2D subunit-containing NMDARs, was the most effective blocker of D-Asp currents observed, at 46 ± 22% block (Fig. 2D and Table 2; P≤ 0.01); L-Glu currents in the Inhibitors,research,lifescience,medical same cells were blocked to a similar degree on average, although the specific proportion of block of the two receptors in individual cells varied from 31% to 77% with a greater proportion of D-Asp current blocked in some cells, while in other cells more L-Glu current was blocked. PPDA block Thiamine-diphosphate kinase of both receptors was reversible. Adding the percentage block of L-GluRs by kynurenate (−65 ± 13%) to that by APV (0%) and PPDA (−46 ± 11%) exceeded the observed block of these receptors by a mixture of kynurenate + APV + PPDA (−76 ± 21%). The same was true for D-AspRs, if considering only APV block and not APV-induced potentiation (Table 2). Figure 3 Antagonists of D-Asp currents at −30 mV. (A and B) Currents in D-Asp (1 mM) in ASW (control) and in ASW with 100 μM APV. Inset B: whole-cell currents in L-Glu (1 mM) in ASW (control) and in ASW plus 100 μM APV. (C) Currents in …
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