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The PLD2-mediated low-level ROS generation by receptor-internalizing or endogenous opioids might be one reason for a lower neurotoxicity compared with noninternalizing opioids under physiologic conditions and this might have implications for analgesic therapy

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One overall difficulty in interpretation of these in vivo studies is the fact that sometimes the ERK1/2 activation occurs in opioid-sensitive neurons and other times is indirect via disinhibition of other neurons or perhaps by activation of ERK1/2 signaling pathways in glia or astrocytes (Eitan et al., 2003