“…The doses were determined based on the previous studies [1,30], and drugs were intraperitoneally injected after 2 hr refeeding. The chronic in ammatory pain was induced by injecting CFA twice (D 0 initial injection and D 7 booster injection) into the hind paw [24], and behavior tests were conducted at 16 days after the rst injection (Fig. 1A).…”
Section: Resultsmentioning
confidence: 99%
“…For refeeding, mice were given normal chow for 2 hr following 24 hr fasting. We used a modi ed CFA-induced chronic in ammatory pain model to prolong pain behaviors for more than 20 days, as previously described [24]. 20 μL of undiluted CFA (Sigma-Aldrich) was injected subcutaneously into the plantar surface of the left hind with a 0.3 mL insulin syringe.…”
Section: Methodsmentioning
confidence: 99%
“…The behavior tests were conducted as described previously [1,24]. For spontaneous pain measurement, mice were acclimated in the cage at least for a week and then adapted in an acrylic observation chamber (size ranges 12×12×12 cm) before the experiment at least three times for three hours.…”
“…The doses were determined based on the previous studies [1,30], and drugs were intraperitoneally injected after 2 hr refeeding. The chronic in ammatory pain was induced by injecting CFA twice (D 0 initial injection and D 7 booster injection) into the hind paw [24], and behavior tests were conducted at 16 days after the rst injection (Fig. 1A).…”
Section: Resultsmentioning
confidence: 99%
“…For refeeding, mice were given normal chow for 2 hr following 24 hr fasting. We used a modi ed CFA-induced chronic in ammatory pain model to prolong pain behaviors for more than 20 days, as previously described [24]. 20 μL of undiluted CFA (Sigma-Aldrich) was injected subcutaneously into the plantar surface of the left hind with a 0.3 mL insulin syringe.…”
Section: Methodsmentioning
confidence: 99%
“…The behavior tests were conducted as described previously [1,24]. For spontaneous pain measurement, mice were acclimated in the cage at least for a week and then adapted in an acrylic observation chamber (size ranges 12×12×12 cm) before the experiment at least three times for three hours.…”
“…Animals were returned to their home cages between the two injections. This dose (10 mg/kg) has previously been shown to block the contribution of endogenous opioid signaling in the tail-withdrawal test ( Rosen et al, 2019 ) and reduce spontaneous pain behaviors initiated by complete Freund’s adjuvant injection ( Lee et al, 2021 ).…”
The mechanisms underlying the transition from acute to chronic pain are unclear but may involve the persistence or strengthening of pain memories acquired in part through associative learning. Contextual cues, which comprise the environment in which events occur, were recently described as a critical regulator of pain memory; both male rodents and humans exhibit increased pain sensitivity in environments recently associated with a single painful experience. It is unknown, however, how repeated exposure to an acute painful unconditioned stimulus in a distinct context modifies pain sensitivity or the expectation of pain in that environment. To answer this question, we conditioned mice to associate distinct contexts with either repeated administration of a mild visceral pain stimulus (intraperitoneal injection of acetic acid) or vehicle injection over the course of three days. On the final day of experiments animals received either an acid injection or vehicle injection prior to being placed into both contexts. In this way, contextual control of pain sensitivity and pain expectation could be tested respectively. When re-exposed to the noxious stimulus in a familiar environment, both male and female mice exhibited context-dependent conditioned analgesia, a phenomenon mediated by endogenous opioid signaling. However, when expecting the presentation of a painful stimulus in a given context, males exhibited conditioned hypersensitivity whereas females exhibited endogenous opioid-mediated conditioned analgesia. These results are evidence that pain perception and engagement of endogenous opioid systems can be modified through their psychological association with environmental cues. Successful determination of the brain circuits involved in this sexually dimorphic anticipatory response may allow for the manipulation of pain memories, which may contribute to the development of chronic pain states.
“…Naloxone or an equivalent volume of PBS vehicle was administered via IP injection to result in a final dose of 10 mg/kg. This dose has previously been shown to block the contribution of endogenous opioid signaling in the tail-withdrawal test (Rosen et al, 2019) and reduce spontaneous pain behaviors initiated by complete Freund’s adjuvant injection (Lee et al, 2021).…”
The mechanisms underlying the transition from acute to chronic pain are unclear but may involve the persistence or strengthening of pain memories acquired in part through associative learning. Contextual cues, which comprise the surrounding environment where events occur, were recently described as a critical regulator of pain memory; both rodents and humans exhibit increased pain sensitivity in environments recently associated with a single painful experience. It is unknown, however, how repeated exposure to an acute painful unconditioned stimulus in a distinct context modifies pain sensitivity or the expectation of pain in that environment. To answer this question, we conditioned mice to associate distinct contexts with either repeated administration of a mild visceral pain stimulus (intraperitoneal injection of acetic acid) or vehicle injection over the course of three days. On the final day of experiments animals received either an acid injection or vehicle injection prior to being placed into both contexts. In this way, contextual control of pain sensitivity and pain expectation could be tested respectively. Both male and female mice developed context-dependent conditional pain tolerance, a phenomenon mediated by endogenous opioid signaling. However, when expecting the presentation of a painful stimulus in a given context, males exhibited conditional hypersensitivity whereas females exhibited endogenous opioid-mediated conditional analgesia. Successful determination of the brain circuits involved in this sexually dimorphic anticipatory response may allow for the manipulation of pain memories, which may contribute to the development of chronic pain states.
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