Editorial: Modulation of Reward Circuitry by Pain and Stress

Modulation of Reward Circuitry by Pain and StressAcute pain is a necessary, physiologically relevant phenomenon that serves as a warning signal for actual or potential tissue damage.It engages a complex and dedicated circuitry within the peripheral and central nervous system to signal and control the sensation of pain.Importantly, it is generally well managed by established analgesics, such as NSAIDs or opioids.Chronic pain, on the other hand, persists beyond any physiologically relevant purpose and becomes a disease state in and of itself.We now understand that chronic pain leads to adaptations in the sensory nervous system that distinguishes it from acute pain-a phenomenon that may contribute to its stubborn persistence in the face of the typical pharmacological armory.One limitation to the classical approach to treatment of pain is the myopic focus on the sensory aspects of pain.However, pain has an equally important affective component.Over long periods of pain stimuli, engagement of affective or reward circuitry can impact underlying mood states, as illustrated by the fact that depression is one of the most common co-morbidities with chronic pain.Moreover, stress, which commonly accompanies on-going pain, can also modulate reward circuitry and has been implicated in prescription analgesic addiction and drug relapse.An emerging question is whether chronic pain can also induce adaptations in reward circuits that contribute to the severity and chronicity of this challenging disease, and the impact this may have on opioid misuse disorders.This Research Topic includes several original research and review articles discussing the impact of chronic pain on reward circuitry.They provide evidence for how chronic pain changes reward circuitry, its interactions with the stress system, and the implications this has for the genesis of psychiatric disorders such as depression and addiction.The review by Dos Santos et al. provides a thorough introduction to the neuroanatomical underpinnings of pain and reward.Evidence is presented from both clinical and preclinical chronic pain studies suggesting significant neuroadaptations within these circuits that may contribute to the chronification of pain and mental co-morbidities such as depression and anxiety.Strategies that restore normal function of these circuits may be beneficial in treating both the sensory and emotional symptoms associated with chronic pain.This review is complemented nicely by the original research article by Wang et al.In this study, the authors explored changes in cortical activation following acute or chronic pain.Using DeltaFosB as a marker of neuronal activation, they found chronic, but not acute pain, stimulated DeltaFosB expression in the medial prefrontal cortex.This provides further evidence for activity-related changes in circuits involved in reward and motivation in chronic pain.The DeltaFosB activation in the medial prefrontal cortex was also observed in a chronic stress model (maternal separation), highlighting the shared pathologies between chronic pain and stress paradigms.Engagement of reward circuits in chronic pain will undoubtedly impact a myriad of pain-related behaviors, including pain hypersensitivity and negative affect.In the review by Gandhi et al., the

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