α2δ-1–Bound N-methyl-d-aspartate receptors are critically involved in chronic morphine exposure–induced activation of N-methyl-d-aspartate receptors at primary afferent terminals. (A, B) Representative current traces show the effect of bath application of 50 μM 2-amino-5-phosphonopentanoic acid (AP5) on the amplitude of evoked monosynaptic excitatory postsynaptic currents (A) and the paired-pulse ratio (B) of a lamina II neuron from a spinal cord slice pretreated with control peptide (1 µM) from a morphine-treated rat. (C) Summary data show the effect of 50 μM AP5 on the mean amplitude (n = 11 neurons) and paired-pulse ratio (n = 11 neurons) of monosynaptic excitatory postsynaptic currents of lamina II neurons from spinal cord slices pretreated with control peptide from morphine-treated rats. (D, E) Representative current traces show no effect of AP5 on the amplitude of evoked monosynaptic excitatory postsynaptic currents (D) or paired-pulse ratio (E) of a lamina II neuron from a spinal cord slice pretreated with α2δ-1Tat peptide (1 µM) from a morphine-treated rat. (F) Summary data show no effect of AP5 on the mean amplitude (n = 11 neurons) or paired-pulse ratio (n = 11 neurons) of evoked monosynaptic excitatory postsynaptic currents of lamina II neurons from spinal cord slices pretreated with α2δ-1Tat peptide from morphine-treated rats. The data are shown as means ± SD. **P < 0.01; ***P < 0.001 versus the baseline. ###P < 0.001 versus the baseline in the morphine + control peptide group.