Abstract
The development of opioid addiction in subjects with established chronic pain is an area that is poorly understood. It is critically important to clearly understand the neurobiology associated with propensity toward conversion to addiction under conditions of chronic pain. To pose the question whether the presence of chronic pain influences motivation to self-administer opioids for reward, we applied a combination of rodent models of chronic mechanical hyperalgesia and opioid self-administration. We studied fentanyl self-administration in mice under three conditions that induce chronic mechanical hyperalgesia: inflammation, peripheral nerve injury, and repeated chemotherapeutic injections. Responding for fentanyl was compared among these conditions and their respective standard controls (naïve condition, vehicle injection or sham surgery). Acquisition of fentanyl self-administration behavior was reduced or absent in all three conditions of chronic hyperalgesia relative to control mice with normal sensory thresholds. To control for potential impairment in ability to learn the lever-pressing behavior or perform the associated motor tasks, all three groups were evaluated for acquisition of food-maintained responding. In contrast to the opioid, chronic hyperalgesia did not interfere with the reinforcing effect of food. These studies indicate that the establishment of chronic hyperalgesia is associated with reduced or ablated motivation to seek opioid reward in mice.
Highlights
Chronic pain is a broadly experienced debilitating condition that represents a significant public health concern [1]
Animals injected with saline (Figure 2B) showed a significant difference in lever pressing between the active and control levers whereas mice injected with complete Freund’s adjuvant (CFA) (Figure 2C) did not
An area under the curve taken from day 8-32, when stable lever pressing was achieved in the saline-injected mice, showed a significant difference in the active vs. the control levers
Summary
Chronic pain is a broadly experienced debilitating condition that represents a significant public health concern [1]. The most effective pain relievers, opioids, are associated with risk of conversion to addiction and diversion from the patients for whom use is intended; these perceived risks constitute a recognized national health problem [1]. The neurobiology of addiction has been considered in the context of opioid use for treatment of chronic pain [3,4]. Studies of opioid reward under conditions of chronic pain have been quite limited in comparison to those conducted in the normal state. This gap is significant because the neurobiology of the central nervous system (CNS) is recognized to be altered under conditions of chronic pain
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