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Basic and clinical neuroscience, 2014
Formalin injection induces nociceptive bahaviour in phase I and II, with a quiescent phase between them. While active inhibitory mechanisms are proposed to be responsible for initiation of interphase, the exact mechanisms which lead to termination of nociceptive response in phase II are not clear yet. Phase II is a consequence of peripheral and central sensitization processes, which can lead to termination of the noxious stimuli responses; 45-60 minutes after formalin injection via possible recruitment of active inhibitory mechanisms which we have investigated in this study. To test our hypothesis, in the first set of experiments, we evaluated nociceptive response after two consecutive injection of formalin (50µL, 2%), with intervals of 5 or 60 minutes. In the next set, formalin tests were carried out in companion with injection of Naloxone Hydrochloride, a non-selective antagonist of opioid receptors, pre-formalin injection and 30 and 45 minutes post formalin injection. While norma...
European Journal of Pharmacology, 2005
To reveal peripheral components of opiate analgesia, effects of loperamide, opioid agonist which does not penetrate the blood-brain barrier, were examined in formalin and acute thermal pain tests in comparison with morphine. Formalin administration induces pain behaviour such licking/biting of injected paw expressed as two phases. The first phase is caused by C-fibre activation due to peripheral stimulation, the second phase attributed to ongoing input from peripheral site, leading to spinal hyperexcitability, which is dependent on N-methyl-D-aspartate (NMDA) receptor activation. Loperamide (3-10 mg/kg) and morphine (6 mg/kg) reduced formalin-induced nociceptive behaviours and these effects were reversed by naloxone methiodide (0.03-10 mg/kg), opioid receptor antagonist which poorly penetrates the blood-brain barrier. Loperamide action was enhanced only by centrally active NMDA receptor antagonists memantine (3 mg/kg) and CGP 37849 (3 mg/kg), but not by NMDA/glycine B receptor antagonists showing weak or no central nervous system (CNS) activity. Present results suggest that central NMDA receptor blockade may be necessary to enhance analgesia induced through peripheral opioid mechanisms in formalin-evoked nociception.
Opioid antagonists and spinal reflexes in the anaesthetized cat Brain Res., 297 (1984) 33–40
Pain, 1985
In barbiturate-anaesthetized cats, intravenous naloxone (0.(}25-0.10 mg/kg) increased thc amplitude of monosynaptic reflexes produccd by electrical stimulation of the nerves to the biceps-scmitendinosus and gastrocnemius muscles and the complex reflexes to electrical stimulation of myelinated afferents of the sural and tibial nerves and reflexes to electrical stimulation of unmyelinated primary afferents of the tibial ncrvc. Increases in reflexes were also produced by the (--)-but not the ( + )-isomer of the opiate antagonist N-furylmethylnormetazocine (both isomers being given in the dose range 0.03-0.20 mg/kg). The doses of naloxone increasing reflexes to C primary afferents had no effect on the responses of some dorsal horn neurones with cutaneous receptive fields to the same stimuli. Thc results suggest that, in anaesthetized cats, inhibition involving opioid peptides at some stage is present on many motoneuroncs. This inhibition may have relevance to animal behaviour after injury.
Brain Research, 1996
The effects of peripheral administration of naloxone and naltrexone on aversive thresholds (freezing and escape reactions) elicited by electrical stimulation of the midbrain tectum were determined. Naloxone caused a significant increase in the freezing and flight thresholds elicited by electrical stimulation in the deep layers of the superior colliculus and of dorsal regions of the periaqueductal grey matter, as compared with controls. These effects were confirmed by the peripheral administration of naltrexone. These findings suggest that opioid receptors can modulate aversive behaviour elicited by midbrain tectum stimulation.
British Journal of Pharmacology, 2001
The effects of intravenous sufentanil and pre-administration of N-methyl-D-aspartate (NMDA) receptor antagonists were tested on a reflex triggered by C-fibre activation. The reflex was elicited by electrical stimulation of the sural nerve and recorded from the ipsilateral biceps femoris muscle in halothane anaesthetized rats either (1) with an intact neuraxis or (2) in which the brain had previously been transected at the level of the obex.All four doses of sufentanil (0.33, 0.6, 1 and 2 μg kg−1) elicited a depression of the reflex in a dose-dependent manner. However, following the expected depression, all doses of sufentanil elicited both facilitation of the reflex and tonic inter-stimulus discharges.The C-fibre reflex was not modified following intravenous ketamine (1 mg kg−1) or (+)-HA966 (5 or 10 mg kg−1) but, when administered 5 min before sufentanil, these drugs enhanced both the extent and the duration of the depression and strongly reduced the facilitations.In the obex-transected rats, the depressive effect of 1 μg kg−1 sufentanil increased, while the facilitation of the C-fibre reflex and the tonic inter-stimulus discharges disappeared. Pre-administration of 10 mg kg−1 (+)-HA966 reinforced and prolonged the depressive effect of sufentanil.These results extend previous studies suggesting the involvement of NMDA receptors in the spinal transmission of nociceptive signals. They illustrate the potential of spinal NMDA receptor blockade to both enhance the analgesic, and prevent the pro-nociceptive, effects of sufentanil.The effects of intravenous sufentanil and pre-administration of N-methyl-D-aspartate (NMDA) receptor antagonists were tested on a reflex triggered by C-fibre activation. The reflex was elicited by electrical stimulation of the sural nerve and recorded from the ipsilateral biceps femoris muscle in halothane anaesthetized rats either (1) with an intact neuraxis or (2) in which the brain had previously been transected at the level of the obex.All four doses of sufentanil (0.33, 0.6, 1 and 2 μg kg−1) elicited a depression of the reflex in a dose-dependent manner. However, following the expected depression, all doses of sufentanil elicited both facilitation of the reflex and tonic inter-stimulus discharges.The C-fibre reflex was not modified following intravenous ketamine (1 mg kg−1) or (+)-HA966 (5 or 10 mg kg−1) but, when administered 5 min before sufentanil, these drugs enhanced both the extent and the duration of the depression and strongly reduced the facilitations.In the obex-transected rats, the depressive effect of 1 μg kg−1 sufentanil increased, while the facilitation of the C-fibre reflex and the tonic inter-stimulus discharges disappeared. Pre-administration of 10 mg kg−1 (+)-HA966 reinforced and prolonged the depressive effect of sufentanil.These results extend previous studies suggesting the involvement of NMDA receptors in the spinal transmission of nociceptive signals. They illustrate the potential of spinal NMDA receptor blockade to both enhance the analgesic, and prevent the pro-nociceptive, effects of sufentanil.British Journal of Pharmacology (2001) 133, 1013–1022; doi:10.1038/sj.bjp.0704148
European Journal of Pharmacology, 2009
This study assesses the effects of peripheral or intrathecal pre-treatment or post-treatment with µ, δ, κ and nociceptin/orphanin FQ (NOP) opioid receptor agonists (morphine, U-50488 [trans-(±)-3,4-dichloro-Nmethyl-N-[2-(1-pyrrolidinyl)cyclohexyl]benzeneacetamide hydrochloride], DADLE [D-Ala2-Leu5-enkephalin] and nociceptin, respectively) on formalin-induced secondary mechanical allodynia and hyperalgesia in rats. 1% Formalin injection produced acute nociceptive behaviors (flinching and licking/lifting) followed by long-term tactile secondary allodynia and hyperalgesia. Neither peripheral (into the formalin-injected paw) nor intrathecal morphine post-treatment reversed formalin-induced secondary allodynia and hyperalgesia. In contrast, morphine pre-treatment prevented the development of these pain behaviors. Intrathecal and peripheral post-but not pre-treatment with U-50488 or DADLE significantly reduced secondary allodynia and hyperalgesia. Interestingly, nociceptin reduced both pain behaviors regardless of the administration site or treatment time. Local antinociceptive effects of morphine, DADLE, U-50488 or nociceptin were blocked by naltrexone, naltrindole, 5-guanidinonaltrindole and [Nphe 1 ]nociceptin(1-13)NH 2 , respectively. These results suggest that the long-term nociceptive behaviors induced by formalin are differentially modulated by selective opioid receptor agonists. In addition, data suggest that peripheral and spinal δ and κ opioid receptors are important when nociceptive behaviors are established. In contrast, µ opioid receptors are more important at the beginning of the injury when the sensory system has not changed. NOP receptors participate diminishing both the development and maintenance of nociceptive behaviors. Results suggest that a barrage of afferent input induced by formalin injection initiates a long-term differential change in peripheral and spinal processing that affect the efficacy of opioid receptor agonists.
Opioid inhibition of formalin-induced changes in plasma extravasation and local blood flow in rats
Pain, 2000
Hindpaw injection of dilute formalin produces brief (Phase 1) and persistent (Phase 2) nociceptive responses in the rat. We recently showed that systemically-administered remifentanil during Phase 1 interacted with peripheral opioid receptors to delay the onset and termination of Phase 2 . To test the hypothesis that opioid inhibition of proin¯ammatory events during Phase 1 contributed to this delay, we evaluated the effects of remifentanil on the time course of formalin-induced in¯ammation. We found that formalin increased paw thickness (edema), plasma extravasation and local blood¯ow within minutes of its injection, i.e. during Phase 1. Each of these responses was blocked during remifentanil administration (30 mg/kg i.v. bolus, followed 90 s later with a 15 mg/kg/min infusion for 13.5 min), indicating that opioids inhibit Phase 1 in¯ammation. Opioid blockade of the blood¯ow response could be reversed with a peripherally-acting opioid antagonist, naloxone methiodide, indicating that remifentanil acted upon peripheral opioid receptors. Although the administration of remifentanil during Phase 1 did not reduce the magnitude of in¯ammatory responses during Phase 2, it did delay the onset and termination of edema during Phase 2. As this corresponds to the effects of remifentanil on nociceptive responses during Phase 2, we suggest that opioid analgesics act upon peripheral sites to inhibit in¯ammation during Phase 1, leading to a delay in the temporal pro®le of in¯ammatory (and likely nociceptive) responses during Phase 2. q 2000 International Association for the Study of Pain. Published by Elsevier Science B.V.
Role of �-opioid receptors in formalin-induced pain behavior in mice
Exp Neurol, 2003
Intraplantar formalin injection is widely used as an experimental model of tonic pain. We investigated the role of endogenous μ-opioid receptor mechanisms in formalin-induced nocifensive behavior in mice. The flinching response induced by formalin (2%, 20 μl) was studied in mice with normal (wild type, n = 8) and absent (homozygous μ-opioid receptor knockout, n = 8) μ-opioid receptor levels. The flinch responses were counted every 5 min for 60 min post-formalin injection. Lumbar spinal cord (L4, 5) was harvested 2 h post-formalin injection to examine c-Fos expression using immunohistochemistry. The effects of naloxone (5 mg/kg, sc) administered 30 min before the intraplantar formalin injection on the flinching response of wild-type mice (n = 7) were also recorded. The second-phase formalin response (10–60 min after formalin) was higher in homozygous μ-opioid receptor knockout mice compared to the wild-type mice (P < 0.01). Naloxone administration in wild-type mice before formalin injection resulted in pain behavior similar to that observed in homozygous μ-opioid receptor knockout mice (P > 0.05). The c-Fos expression induced by formalin injection in the knockout mice was not different from that observed in wild-type mice. Our results suggest that the endogenous μ-opioid system is activated by intraplantar formalin injection and exerts a tonic inhibitory effect on the pain behavior. These results suggest an important modulatory role of endogenous μ-opioid receptor mechanisms in tonic pain states.
Role of μ-opioid receptors in formalin-induced pain behavior in mice
Experimental Neurology, 2003
Intraplantar formalin injection is widely used as an experimental model of tonic pain. We investigated the role of endogenous A-opioid receptor mechanisms in formalin-induced nocifensive behavior in mice. The flinching response induced by formalin (2%, 20 Al) was studied in mice with normal (wild type, n = 8) and absent (homozygous A-opioid receptor knockout, n = 8) A-opioid receptor levels. The flinch responses were counted every 5 min for 60 min post-formalin injection. Lumbar spinal cord (L4, 5) was harvested 2 h post-formalin injection to examine c-Fos expression using immunohistochemistry. The effects of naloxone (5 mg/kg, sc) administered 30 min before the intraplantar formalin injection on the flinching response of wild-type mice (n = 7) were also recorded. The second-phase formalin response (10 -60 min after formalin) was higher in homozygous A-opioid receptor knockout mice compared to the wild-type mice ( P < 0.01). Naloxone administration in wild-type mice before formalin injection resulted in pain behavior similar to that observed in homozygous A-opioid receptor knockout mice ( P > 0.05). The c-Fos expression induced by formalin injection in the knockout mice was not different from that observed in wild-type mice. Our results suggest that the endogenous A-opioid system is activated by intraplantar formalin injection and exerts a tonic inhibitory effect on the pain behavior. These results suggest an important modulatory role of endogenous A-opioid receptor mechanisms in tonic pain states. D