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. 2005 Mar 23;25(12):3192–3198. doi: 10.1523/JNEUROSCI.4585-04.2005

Figure 5.

Figure 5.

Induction of DOPr function by long-term morphine treatment requires MOPrs and β-arrestin-2. Neurons from MOPr-/- or βarr2-/- do not develop DOPr-mediated presynaptic inhibition after chronic treatment with morphine. Knock-out mice and their wild-type littermates were treated with the standard morphine treatment protocol and probed for DOPr-mediated presynaptic inhibition of GABA release after washout of morphine for 1 h in vitro. Six of 10 neurons tested from wild-type mice expressing MOPr responded to DELT, but no PAG neurons tested from MOPr-/- mice responded to DELT. Wild-type littermates expressing βarr2 (βarr2+/+) demonstrated DOPr-mediated inhibition of GABA release in five of nine neurons after morphine treatment, but no neurons tested from βarr2-/- mice responded to DELT (0 of 9; p < 0.05 vs wild-type littermates; χ2 test). Data from vehicle and morphine-treated C57BL/6J mice are shown for comparison. Numbers within the bars indicate the number of neurons that responded or did not respond to DELT application.