Hyperalgesia induced by non-noxious stress in the rat

Vidal, Catherine; Jacob, J.

doi:10.1016/0304-3940(82)90232-4

Cited by 42 publications

(23 citation statements)

References 13 publications

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“…These findings suggest that there may be two functionally distinct pro-and antinociceptive descending pathways from the ventrolateral orbitofrontal cortex to the PAG, which may be activated differentially according to the way the stimulus is perceived by the individual. In support of this idea, studies in male rats have shown that although exposure to a non-noxious stress induced hyperalgesia (Vidal and Jacob, 1982;J rum, 1988), a more severe stress induced an increase in pain threshold (Rizzi et al, 2001;Vendruscolo et al, 2004). The mild stressor used in this study would therefore be expected to activate the pro-nociceptive pathways from the PAG.…”

Section: Stress-induced Hyperalgesia In Female Ratssupporting

confidence: 54%

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Devall¹,

Lovick²

2010

Neuropsychopharmacol

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The effect of acute exposure to mild anxiogenic stress on cutaneous nociceptive threshold was investigated in female Wistar rats at different stages of the estrous cycle. Baseline tail flick latencies did not change significantly during the cycle. However after brief exposure to vibration stress (4 Hz for 5 min), rats in late diestrus, but not at other cycle stages, developed a hyperalgesia (decrease in tail flick latency). Animals in late diestrus revealed a more than fivefold increase in the density of Fos-like immunoreactive nuclei in the dorsolateral, lateral, and ventrolateral columns in the caudal half of the periaqueductal gray matter (PAG). There was no change in the density of Fos-like immunoreactive nuclei in the PAG in rats in estrus and early diestrus, although rats in proestrus showed a smaller (50%) but significant increase. Rats undergoing withdrawal from a progesterone dosing regimen (5 mg/kg i.p. twice daily for 6 days) designed to mimic the fall in progesterone that occurs naturally during late diestrus, exhibited a stress-induced hyperalgesia that was similar to animals in late diestrus and a significant increase in Fos-positive cells in the PAG. We suggest that falling levels of progesterone during late diestrus may be a predisposing factor for the development of stress-induced hyperalgesia, which is linked to differential activation of descending pain control circuits in the PAG. Similar changes in women, when progesterone levels fall during the late luteal phase of the menstrual cycle, may contribute to the development of premenstrual symptoms that include increased anxiety and hyperalgesia.

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Section: Stress-induced Hyperalgesia In Female Ratssupporting

confidence: 54%

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Devall¹,

Lovick²

2010

Neuropsychopharmacol

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“…Among various CNS systems involved in producing stressinduced analgesia (SIA), endogenous opioids play a critical role (Akil et al, 1976;Lewis et al, 1980). However, hyperalgesia following stress has also been reported in animals (Vidal and Jacob, 1982) especially when stress is repeated for a long time (Satoh et al, 1992;da Silva Torres et al, 2003;Bradesi et al, 2005;Khasar et al, 2005;Gameiro et al, 2006). Unlike SIA, the mechanisms involved in stressinduced hyperalgesia (SIH) are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Non-Nociceptive Environmental Stress Induces Hyperalgesia, Not Analgesia, in Pain and Opioid-Experienced Rats

Rivat¹,

Laboureyras²,

Laulin

et al. 2007

Neuropsychopharmacol

117

116

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It is well admitted that stress induces analgesia (SIA) via endogenous opioid release. However, there is evidence that stressful events play a role in the pathogenesis of pain, but little is known about mechanisms underlying such pain vulnerability. Previous studies reported that a single opioid exposure activates NMDA-dependent pronociceptive systems leading to long-term pain vulnerability after analgesia. Here, we studied whether prior inflammatory pain or/and opioid experiences may favour the development of pain vulnerability after nonnociceptive environmental stress (NNES). Nociceptive threshold (NT) changes were evaluated by paw pressure vocalization test. By contrast to discrete SIA observed in naive rats, 1 h stress induced hyperalgesia (SIH) for several hours (15-65% NT decrease) in pain and opioid experienced rats. Repetition of NNES induced an 18-to 22-fold SIH enhancement (3-4 days), whereas SIA decreased. SIH was still observed 4 months after pain and opioid experiences. This phenomenon is referred to as latent pain sensitization. Furthermore, a fentanyl ultra-low dose (ULD, 50 ng/kg) administration, mimicking SIA in naive rats, induced hyperalgesia (65% NT decrease, 4 h), not analgesia, in pain and opioid-experienced rats. This indicates that low levels of opioids induce opposite effects, that is analgesia vs hyperalgesia dependent on prior life events. In pain and opioid-experienced rats, NMDA receptor antagonists, ketamine or BN2572, completely prevented hyperalgesia when injected just before NNES or fentanyl ULD. This latent pain sensitization model may be important for studying the transition from acute to chronic pain and individual differences in pain vulnerability associated with prior life events.

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“…Most studies show that stress suppresses pain sensation (Guillemin et al 1977;Madden et al 1977;Lafrance et al 2010;HeidariOranjaghi et al 2012). However, in contrast to suppressive effects on nociception, some studies indicate that some types of stress induce hyperalgesia (Vidal and Jacob 1982). Rivat et al found that non-nociceptive environmental stress induced hyperalgesia in pain and opioid-treated rats (Rivat et al 2007).…”

Section: Discussionmentioning

confidence: 97%

Role of spinal GABAA receptor reduction induced by stress in rat thermal hyperalgesia

Weiying

Wang

et al. 2014

Exp Brain Res

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The mechanisms underlying stress-induced hyperalgesia (SIH) remain poorly understood. Recent findings have provided strong evidence indicating that SIH could be related, at least in part, to alterations in spinal cord GABA activity. In the present study, we first investigated how acute restraint stress impacted pain responses as assessed using the tail flick immersion test. These results showed that rats developed hyperalgesia at 6 h after being subjected to 1-h acute restraint stress. Second, we measured the activation of spinal neurons and alterations in expression of GABAA receptor β2 and β3 subunits as related to stress-induced hyperalgesia. Results from Western blot and immunofluorescence assays showed that c-fos protein increased in the dorsal horn of the lumbar spinal cord and GABAA receptor β2 and β3 subunit proteins decreased significantly at 6 h after exposure to 1 h of acute restraint stress. Finally, the effects of spinal GABAA receptor alteration on SIH were evaluated. These results showed that intrathecal administration of muscimol inhibited hyperalgesia induced by stress while bicuculline enhanced hyperalgesia in the control groups. Taken together, the present data reveal that GABAA receptor β2 and β3 decrease following 1 h of acute restraint stress and may play a critical role in SIH.

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Hyperalgesia induced by non-noxious stress in the rat

Cited by 42 publications

References 13 publications

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Non-Nociceptive Environmental Stress Induces Hyperalgesia, Not Analgesia, in Pain and Opioid-Experienced Rats

Role of spinal GABAA receptor reduction induced by stress in rat thermal hyperalgesia

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