The maintenance of individual differences in the sensitivity of acute and neuropathic pain behaviors to electroacupuncture in rats

Kim, Sun Kwang; Moon, Hak Jin; Park, Jung Hyuk; Lee, Giseog; Shin, Monica; Hong, Min; Bae, Hyunsu; Jin, Yongfeng; Min, Byung-Il

doi:10.1016/j.brainresbull.2007.07.006

Cited by 26 publications

(29 citation statements)

References 15 publications

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“…Furthermore, CCK1 receptor expression is higher in low responders than high responders to 2-Hz EA treatment (34). Similarly, the analgesic effect induced by 2-Hz EA is enhanced in CCK1 receptor-deficient rats compared with the wild-type rats (31,35). None of these experiments actually prove that CCK is the cause of decreased responsiveness to acupuncture, since they rely strictly on associations.…”

Section: Discussionmentioning

confidence: 89%

“…CCK containing neurons and receptors are localized in the brain stem, although the rVLM has not previously been examined specifically (4, 51-53). Several studies have sug- gested that the CCK system may contribute to the mechanism underlying decreased responsiveness to EA-induced analgesia (25,31,32,34,35,63,76). For example, CCK1 and CCK2 receptor gene expression in the hypothalamus has been demonstrated to have an inverse relationship with the individual variations to analgesia during high-frequency (100 Hz) EA in rats (32).…”

Section: Discussionmentioning

confidence: 97%

“…Exogeneous CCK injected intracerebroventricularly was used in one study (25). Other studies have relied on molecular rather than physiological evidence (31,32,34,35,76). A single study evaluating low responders has shown that reducing tissue levels of CCK in the cortex, hippocampus, and midbrain is associated with an increase in the responsiveness to EA analgesia (63).…”

mentioning

confidence: 98%

“…CCK-8 in the rVLM modulates sympathetic outflow (61,62). This peptide antagonizes the opioid regulation of pain (26), mood disorders (27), as well as acupuncture's action through stimulation of CCK1 and CCK2 receptors (25,31,32,34,35,63,76). In the past two decades, the CCK system has been shown to reduce responsiveness to the analgesic effect of EA (25,31,32,34,35,63,76).…”

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confidence: 99%

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Electroacupuncture modulation of reflex hypertension in rats: role of cholecystokinin octapeptide

Tjen‐A‐Looi

Guo

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Acupuncture or electroacupuncture (EA) potentially offers a nonpharmacological approach to reduce high blood pressure (BP). However, ~70% of the patients and animal subjects respond to EA, while 30% do not. EA acts, in part, through an opioid mechanism in the rostral ventrolateral medulla (rVLM) to inhibit sympathoexcitatory reflexes induced by gastric distention. CCK-8 opposes the action of opioids during analgesia. Therefore, we hypothesized that CCK-8 in the rVLM antagonizes EA modulation of sympathoexcitatory cardiovascular reflex responses. Male rats anesthetized with ketamine and α-chloralose subjected to repeated gastric distension every 10 min were examined for their responsiveness to EA (2 Hz, 0.5 ms, 1-4 mA) at P5-P6 acupoints overlying median nerve. Repeated gastric distension every 10 min evoked consistent sympathoexcitatory responses. EA at P5-P6 modulated gastric distension-induced responses. Microinjection of CCK-8 in the rVLM reversed the EA effect in seven responders. The CCK1 receptor antagonist devazepide microinjected into the rVLM converted six nonresponders to responders by lowering the reflex response from 21 ± 2.2 to 10 ± 2.9 mmHg (first vs. second application of EA). The EA modulatory action in rats converted to responders with devazepide was reversed with rVLM microinjection of naloxone (n = 6). Microinjection of devazepide in the absence of a second application of EA did not influence the primary pressor reflexes of nonresponders. These data suggest that CCK-8 antagonizes EA modulation of sympathoexcitatory cardiovascular responses through an opioid mechanism and that inhibition of CCK-8 can convert animals that initially are unresponsive to EA to become responsive.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 98%

mentioning

confidence: 99%

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Electroacupuncture modulation of reflex hypertension in rats: role of cholecystokinin octapeptide

Tjen‐A‐Looi

Guo

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, there have been many reports showing individual differences in the sensitivity to EA analgesia, which cause experimental and clinical difficulties: About 30-40% of rats were insensitive to EA in an acute thermal pain test, tail flick latency (TFL) test [5,8,9]. The similar results could be observed in the rat models of inflammatory and neuropathic pain [10,11]. …”

Section: Introductionmentioning

confidence: 86%

Expression levels of the hypothalamic AMPK gene determines the responsiveness of the rats to electroacupuncture-induced analgesia

Kim

Sun

Yoon

et al. 2014

BMC Complement Altern Med

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BackgroundAlthough electroacupuncture (EA) relieves various types of pain, individual differences in the sensitivity to EA analgesia have been reported, causing experimental and clinical difficulties. Our functional genomic study using cDNA microarray identified that 5’-AMP-activated protein kinase (AMPK), a well-known factor in the regulation of energy homeostasis, is the most highly expressed gene in the hypothalamus of the rats that were sensitive to EA analgesia (“responder”), as compared to the rats that were insensitive to EA analgesia (“non-responder”). In this study, we investigated the causal relationship between the hypothalamic AMPK and the individual variation in EA analgesia.MethodsSprague-Dawley (SD) rats were divided into the responder and the non-responder groups, based on EA-induced analgesic effects in the tail flick latency (TFL) test, which measures the latency of the tail flick response elicited by radiant heat applied to the tail. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to quantify the expression levels of AMPK mRNA in the hypothalamus of the responder and non-responder rats. Further, we examined whether viral manipulation of the AMPK expression in the hypothalamus modulates EA analgesia in rats.ResultsThe real-time RT-PCR analysis showed that mRNA expression levels of AMPK in the hypothalamus of the responder rats are significantly higher than those of the non-responder rats, validating the previous microarray results. Microinjection of dominant negative (DN) AMPK adenovirus, which inhibits AMPK activity, into the rat hypothalamus significantly attenuates EA analgesia (p < 0.05), whereas wild type (WT) AMPK virus did not affect EA analgesia (p > 0.05).ConclusionsThe present results demonstrated that levels of AMPK gene expression in the rat hypothalamus determine the individual differences in the sensitivity to EA analgesia. Thus, our findings provide a clinically useful evidence for the application of acupuncture or EA for analgesia.

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Glial–Neuronal Interactions in Electroacupuncture Analgesia

Cao

Zhang

2012

Current Research in Acupuncture

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The maintenance of individual differences in the sensitivity of acute and neuropathic pain behaviors to electroacupuncture in rats

Cited by 26 publications

References 15 publications

Electroacupuncture modulation of reflex hypertension in rats: role of cholecystokinin octapeptide

Electroacupuncture modulation of reflex hypertension in rats: role of cholecystokinin octapeptide

Expression levels of the hypothalamic AMPK gene determines the responsiveness of the rats to electroacupuncture-induced analgesia

Glial–Neuronal Interactions in Electroacupuncture Analgesia

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