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. 2009 Jun 3;29(22):7349–7358. doi: 10.1523/JNEUROSCI.0381-09.2009

Figure 4.

Figure 4.

κ-Opioid inhibition persists after antagonism of presynaptic Ca2+ channels. A, Evoked glutamate release onto MNCs is mediated mostly by N-type Ca2+ channels as bath application of the N-type Ca2+ channel blocker ω-conotoxin GVIA (1 μm, 5 min) reduced the charge transfer of the EPSC by 77 ± 6% (n = 8, p = 0.01). Sample EPSCs are from control, 15 and 30 min after ω-conotoxin. B, Blocking P/Q-type channels with ω-agatoxin IVA (200 nm, 10 min) reduced the EPSC charge transfer by only 16 ± 12% (n = 6, p = 0.21). Sample EPSCs are from control, 15 and 30 min after ω-agatoxin. C–F, When U69593 was applied to cells that had previously had either N- or P/Q-type channels blocked, there was no occlusion of the inhibitory effect of the κ-opioid agonist. C and D are data from the same cell. Traces in C were taken in control, 15 min after ω-conotoxin and 10 min after subsequent application of U69593. The inset in E shows the charge transfer after ω-conotoxin normalized to 100%.