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. 2012 Jun 7;287(30):25073–25085. doi: 10.1074/jbc.M112.378737

FIGURE 2.

FIGURE 2.

Potentiation of glutamatergic input to spinal dorsal horn neurons through increased activity of NMDARs at primary afferent terminals by chronic morphine. A, original recordings show the effect of 50 μm AP5 on monosynaptic AMPAR-EPSCs of the lamina II neuron evoked from the dorsal root in a vehicle-treated and a morphine-treated rat (recorded with and without 1 mm MK-801 in the pipette solution). B, group data show the effect of 50 μm AP5 on the mean amplitude of evoked AMPAR-EPSCs of lamina II neurons in vehicle-treated (n = 9 neurons) as well as morphine-treated rats recorded without MK-801 (n = 11 neurons) or with MK-801 (n = 9 neurons). C, AP5-produced inhibition of the EPSC amplitude in morphine-treated rats was associated with a decreased paired-pulse ratio (n = 11 neurons). *, p < 0.05 when compared with respective base-line controls. #, p < 0.05 when compared with base-line controls in vehicle-treated group.