Long‐lasting increased pain sensitivity in rat following exposure to heroin for the first time

Laulin, Jean‐Paul; Larcher, A.; Célèrier, Evelyne; Moal, Michel Le; Simonnet, Guy

doi:10.1046/j.1460-9568.1998.00083.x

Cited by 150 publications

(96 citation statements)

References 15 publications

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“…For example, when injected shortly after administration of a dose of morphine or fentanyl, naloxone both abolishes the acute opiate-induced increase in nociceptive threshold and also reduces it to below basal value (hyperalgesia). This hyperalgesia can be blocked by noncompetitive NMDA receptor antagonists suggesting a critical role for glutamatergic systems (Celerier et al 1999;Larcher et al 1998;Laulin et al 1998). This hyperalgesia and allodynia (b-process) also sensitizes both with repeated drug administration and over time leading to an apparent tolerance.…”

mentioning

confidence: 99%

Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,564

1,962

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This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drugtaking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to BACKGROUNDDrug addiction is a chronically relapsing disorder that is defined by two major characteristics: a compulsion to take the drug with a narrowing of the behavioral repertoire toward excessive drug intake, and a loss of control in limiting intake (American Psychiatric Association 1994; World Health Organization 1992). An important challenge for neurobiological research is to understand the neuroadaptive differences between controlled drug use and loss of control, and by extension, the molecular, cellular and system processes that lead to addiction (Koob and Le Moal 1997).Animal models are critical for understanding the neuropharmacological mechanisms involved in the development of addiction. While there are no complete animal models of addiction, animal models do exist for many elements of the syndrome. These elements can be derived from symptoms or diagnostic criteria for addiction or conceptual frameworks such as different sources of reinforcement (American Psychiatric Association 1994; World Health Organization 1992). Linking neu- 24 , NO . 2 ropharmacological events to animal models can occur at multiple levels of analysis -molecular, cellular and system -and it will only be the integration of these changes across dimensions of analysis that will allow a full understanding of the neurobiology of drug addiction.Advances in neuroscience research are rapidly unr...

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mentioning

confidence: 99%

Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,564

1,962

View full text Add to dashboard Cite

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“…There is some evidence that analgesic effects, due to repeated opioid dosing, may result in the development of hyperalgesia, the magnitude and duration of which is dosedependent. 6,12,19,31 Further evidence of this phenomenon originates from experimental studies that report hyperalgesia lasting for several days after heroin or fentanyl administration. 32,33 The concept of general balanced anesthesia is defined by the co-administration of several pharmacological agents, so as to enhance their beneficial effects while reducing the side effects of individual drugs administered in high doses.…”

Section: Discussionmentioning

confidence: 99%

“…1,4 Paradoxically, opioids have also been reported to induce hyperalgesia and allodynia via an activation of the same NMDA receptors. 5,6 Enhanced hyperalgesia was observed for several days after injections of high doses of fentanyl were administered to animals that were subjected to inflammatory or surgical pain in response to nociceptive inputs. 7,8 In human volunteers, other opioids, such as remifentanil, induced not only analgesia but also hyperlagesia once the medication was discontinued.…”

Section: Résumémentioning

confidence: 99%

Effects of sevoflurane on carrageenan- and fentanyl-induced pain hypersensitivity in Sprague-Dawley rats

Richebé

Rivalan

Rivat

et al. 2008

Can J Anesth/J Can Anesth

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Purpose Opioids are widely used for anesthesia but paradoxically induce postoperative pain hypersensitivity via N-methyl-D-aspartate (NMDA) receptor modulation. Sevoflurane effects on opioid-induced hyperalgesia have not been yet evaluated in vivo. Nevertheless, some experimental in vitro studies reported anti-NMDA receptor properties for sevoflurane. The aim of this study was to evaluate sevoflurane effects on fentanyl-induced hyperalgesia in opioid-naive rats and in rats with inflammatory pain. Methods Sevoflurane effects on hyperalgesia were evaluated in Sprague-Dawley rats: opioid-naive rats, rats treated with fentanyl (4 9 60 lg kg -1 ) and rats with inflammatory pain (carrageenan) treated with fentanyl (4 9 60 lg kg -1 ). On day zero, subcutaneous fentanyl injections were administered and inflammatory pain was induced with one carrageenan injection in one hind paw. Rats were exposed to low concentrations of sevoflurane (1.0 or 1.5%) on day zero prior to fentanyl injections and inflammatory pain induction, and for the duration of the fentanyl analgesic effect. The nociceptive threshold (Randall-Selitto test) was evaluated daily for 7 days. On day seven, naloxone was injected and the nociceptive threshold was assessed 5 min later. Results In rats without inflammatory pain but treated with fentanyl on day zero, sevoflurane 1.0% reversed the early (day zero) and long-lasting (day zero to day three) hyperalgesia classically described after high-doses of fentanyl (P \ 0.05). This sevoflurane concentration antagonized the hyperalgesia induced by naloxone on day seven (P = 0.33). In a second experiment in rats with inflammatory pain, exposure to low concentrations of sevoflurane (1.0 and 1.5%) did not reduce fentanyl-induced hyperalgesia (P [ 0.05), but nevertheless antagonized the naloxone induced hyperalgesia on day seven (P = 0.061). Conclusion Relatively low sevoflurane concentrations (1.0%) reverse fentanyl-induced hyperalgesia in rats without inflammatory pain. Nevertheless, the lack of effect of sevoflurane concentrations of 1.0% and 1.5% to oppose hyperalgesia following high-dose fentanyl and inflammatory pain suggests that sevoflurane anti-hyperalgesic properties are weak. RésuméObjectif Les opioı¨des sont largement utilise´s en anesthe´sie mais induisent paradoxalement une hypersensibiliteṕ ostope´ratoire a`la douleur via une modulation des re´cepteurs N-me´thyl-D-aspartate (NMDA). Les effets du

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“…This study did not differentiate whether the prolonged allodynia is a result of 1) a delay in the maturation of paw withdrawal thresholds or 2) the presence of prolonged withdrawalassociated allodynia. Hypersensitivity long into the abstinent period has been previously reported in adult rats following heroin or fentanyl (Laulin et al, 1998, Celerier et al, 2000, Celerier et al, 2001. At the neural level, prolonged excitation persist long after abstinence in dorsal root ganglion cultures exposed to chronic morphine (Crain and Shen, 1995).…”

Section: Withdrawal-associated Mechanical Allodyniamentioning

confidence: 92%

“…This is similar to a previous report that a single acute dose of heroin produces an early allodynia of short duration and a second longer lasting allodynia. The magnitude and duration of this second allodynia is dependent upon the dose of heroin (Laulin et al, 1998). Thus, possibly higher doses of morphine might be required in young rats to produce a second longer lasting allodynia as compared to infant rats.…”

Section: Withdrawal-associated Mechanical Allodyniamentioning

confidence: 99%

Tolerance, opioid-induced allodynia and withdrawal associated allodynia in infant and young rats

Zissen,

Zhang,

McKelvy

et al. 2007

Neuroscience

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Our laboratory has previously characterized age-dependent changes in nociception upon acute morphine withdrawal. This study characterizes changes in mechanical and thermal nociception following acute, intermittent, or continuous morphine administration in infant (postnatal day 5-8) and young (postnatal day 19-21). Morphine was given as a single acute administration (AM), intermittently twice a day for 3 days (IM), or continuously for 72 hours via a subcutaneous pump implanted (CM). AM did not produce long-term changes in mechanical or thermal nociception in either infant or young rats. CM produced changes in mechanical nociception that included the development of tolerance, opioid-induced mechanical allodynia and withdrawal-associated mechanical allodynia in young rats, but only tolerance and a prolonged withdrawal-associated mechanical allodynia in infant rats. IM produced withdrawal-associated mechanical allodynia in both infant and young rats. Measuring paw withdrawal responses to thermal stimuli, infant and young rats showed tolerance without opioid-induced thermal hyperalgesia or withdrawal-associated thermal hyperalgesia following CM. In contrast to CM, withdrawal-associated thermal hyperalgesia was seen in both ages following IM. In conclusion, CM versus IM differentially modified mechanical and thermal nociception, suggesting that opioid-dependent thermal hyperalgesia and mechanical allodynia can be dissociated from each other in infant and young rats. Furthermore, tolerance, opioidinduced hypersensitivity, and withdrawal-associated hypersensitivity are age-specific and may be mediated by distinct mechanisms.Keywords morphine withdrawal; spinal cord; allodynia; hyperalgesia; neonatal rat It has long been recognized that morphine exerts two paradoxical actions on the adult nervous system: the inhibition of pain processing manifested as analgesia and the facilitation of nociceptive sensitivity manifested as allodynia and hyperalgesia (Bederson et al., 1990, Kim et al., 1990, Kaplan and Fields, 1991. This facilitation of nociceptive sensitivity can be observed in as little as 20 min post-morphine administration by precipitating withdrawal with Corresponding Author: Sarah M. Sweitzer, PhD, Department of Pharmacology, Physiology, Neuroscience, University of South Carolina School of Medicine, Columbia, SC 29208, Phone: (803) Fax: (803) 733-1523 Email: sweitzer@med.sc.edu. Section Editor: Dr. Donna Hammond Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 January 5. (Bede...

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Long‐lasting increased pain sensitivity in rat following exposure to heroin for the first time

Cited by 150 publications

References 15 publications

Drug Addiction, Dysregulation of Reward, and Allostasis

Drug Addiction, Dysregulation of Reward, and Allostasis

Effects of sevoflurane on carrageenan- and fentanyl-induced pain hypersensitivity in Sprague-Dawley rats

Tolerance, opioid-induced allodynia and withdrawal associated allodynia in infant and young rats

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