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. 2006 Oct 26;578(Pt 1):143–157. doi: 10.1113/jphysiol.2006.116178

Figure 3. σR-1 agonist modulation of NMDAR currents does not depend on Ca2+ influx via T- and L-type Ca2+ channels or Ca2+ release from the intracellular stores.

Figure 3

A, normalized NMDAR current amplitudes (%) are plotted as a function of time. Each point (one every minute; mean ± s.e.m.) is the average of 6 points (stimulations every 10 s). The application of (+)pentazocine (1 μm; black bar) caused an increase in the amplitude of the NMDAR currents when the CA1 pyramidal cells were recorded in presence of mibefradil (10 μm; ▴ n = 5), nicardipine (5 μm; ○; n = 4), CPA (30 μm; □; n = 4) and ryanodine (10 μm; ▪; n = 4), dotted bar. B, examples of traces of the NMDAR currents measured at the time points indicated in A (a and b) are shown for mibefradil, nicardipine, CPA and ryanodine. Each trace is an average of 20 traces. C, histogram showing the average of the enhancing effect of (+)pentazocine on NMDAR currents when the CA1 pyramidal cells are recorded in control (no additional drug; n = 12), in presence of mibefradil (n = 5), nicardipine (n = 4), CPA (n = 4) and ryanodine (n = 4). All the values are means ± s.e.m.