Interaction between histamine and morphine at the level of the hippocampus in the formalininduced orofacial pain in rats

Tamaddonfard, Esmaeal; Erfanparast, Amir; Farshid, Amir Abbas; Khalilzadeh, Emad

doi:10.1016/s1734-1140(11)70508-4

Cited by 23 publications

(34 citation statements)

References 42 publications

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“…Thus, the combinations that enhance opioid analgesic efficacy (e.g., synergism) include association with norepinephrine transport modulators, anti-inflammatory drugs, calcium channels a 2 -d ligands, local anesthetics, a 2 -adrenergic agonists, calcium channel blockers, cannabinoids, GABA B agonists, glial inhibitors, histamine and venlafaxine [4,21,27].…”

Section: Discussionmentioning

confidence: 99%

Systemic synergism between codeine and morphine in three pain models in mice

Miranda

Noriega

Zepeda

et al. 2013

Pharmacological Reports

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Abstract:Background: The combination of two analgesic agents offers advantages in pain treatment. Codeine and morphine analgesia is due to activation of opioid receptor subtypes. Methods: This study, performed in mice using isobolographic analysis, evaluated the type of interaction in intraperitoneal (ip) or intrathecal (it) coadministration of codeine and morphine, in three nociceptive behavioral models. Results: Intrathecal morphine resulted to be 7.5 times more potent than ip morphine in the writhing test, 55.6 times in the tail flick test and 1.7 times in phase II of the orofacial formalin test; however, in phase I of the same test ip was 1.2 times more potent than it morphine. Intrathecal codeine resulted being 3.4 times more potent than ip codeine in the writhing test, 1.6 times in the tail flick test, 2.5 times in phase I and 6.7 times in phase II of the orofacial formalin test. Opioid coadministration had a synergistic effect in the acute tonic pain (acetic acid writhing test), acute phasic pain (tail flick test) and inflammatory pain (orofacial formalin test). The interaction index ranged between 0.284 (writhing ip) and 0.440 (orofacial formalin phase II ip). Conclusion: This synergy may relate to the different pathways of pain transmission and to the different intracellular signal transduction. The present findings also raise the possibility of potential clinical advantages in combining opioids in pain management. Key words: opioids, algesiometer tests, isobolographic analysis, synergismAbbreviations: DOR -delta opioid receptor, ED # -dosage that produced 50% of MPE, I.I. -interaction index, ipintraperitoneal, it -intrathecal, KOR -k opioid receptor, MPE -maximum possible effect, MOR -µ opioid receptor, NSAIDs -nonsteroidal anti-inflammatory drugs, NOP -nociceptin opioid receptor, SEM -standard mean error

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Section: Discussionmentioning

confidence: 99%

Systemic synergism between codeine and morphine in three pain models in mice

Miranda

Noriega

Zepeda

et al. 2013

Pharmacological Reports

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“…Sensory afferents associated with itch stimulate the histaminergic system in the tuberomammillary nucleus of the hypothalamus [215]. These neurons send axonal projections throughout the CNS.…”

Section: The Physiology and Relevance Of Dry Needling Distal Pointsmentioning

confidence: 99%

“…More specifically, histamine receptors (H1 and H2) have been found in the limbic system, to include the hippocampus, the periaqueductal grey and raphe nuclei [216]. General intracerebralventricular injections and specific microinjections of histamine into the periaqueductal grey and raphe nuclei all had antinociceptive effects in animal models [215]. Tamaddonfard et al further demonstrated a synergistic effect of morphine and histamine in the hippocampus [215].…”

Section: The Physiology and Relevance Of Dry Needling Distal Pointsmentioning

confidence: 99%

“…General intracerebralventricular injections and specific microinjections of histamine into the periaqueductal grey and raphe nuclei all had antinociceptive effects in animal models [215]. Tamaddonfard et al further demonstrated a synergistic effect of morphine and histamine in the hippocampus [215].…”

Section: The Physiology and Relevance Of Dry Needling Distal Pointsmentioning

confidence: 99%

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Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Butts¹,

Dunning²

2016

Int J Phys Med Rehabil

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There are a number of biochemical, biomechanical, endocrinological and neurovascular mechanisms underpinning the anti-nociceptive and anti-inflammatory effects of dry needling (DN). While myofascial trigger points likely play a role in peripheral pain, a diagnostic tool for localizing them has not been validated, and DN studies that have targeted trigger points to elicit localized twitch responses have reported mixed results. Therefore, the mechanism responsible for DN-mediated analgesia may be more complicated. DN activates opioid-based pain reduction, mediated by endogenous cannabinoids and the sympathetic nervous system, and non-opioid pain relief via serotonin and norepinephrine from the brain stem. DN also triggers the hypothalamic-pituitary-adrenal axis centrally and the corticotropin releasing hormone-proopiomelanocortin-corticosteroid axis locally to inhibit cox-2, reducing inflammatory cytokines. Recent studies demonstrate that DN combined with mechanical and/or electrical stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels, to include TRPV, ASIC, TTX and P2X/Y. Electrical DN (EDN) stimulates immune cells, fibroblasts and keratinocytes to release CGRP and substance-P, altering the stimulation of TTX receptors to reverse hyperalgesia. It also encourages the supraoptic nucleus to release oxytocin to quiet ASIC receptors peripherally and stimulate opioid interneurons spinally. Moreover, EDN inhibits ERK1/2 kinase pathways of inflammation in the spinal cord and stimulates Aδ fibers and N/OFQ to reverse C-fiber mediated central changes. Mechanotransduction of fibroblasts and peripheral nerves via TRPV1 and P2X/Y-mediated intracellular Ca 2+ wave propagation and subsequent activation of the nucleus accumbens inhibits spinal pain transmission via glycinergic and opioidergic interneurons. The increased ATP is metabolized to adenosine, which activates P1 purinergic receptors, events considered key to DN analgesia and rho kinase-based tissue remodeling. Mechanotransduction-mediated release of histamine further explains analgesia secondary to needling points distal to pain. DN-mediated analgesia is dependent on a number of synergistic physiologic events involving biochemical and mechanical processes in neural, connective and muscle tissue.

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“…It is well known that opioid system, through mu, delta, and kappa receptors, mediates local peripheral, spinal, and supraspinal mechanisms of pain and analgesia (Kanjhan 1995;Stein and Zollner 2009;Bodnar 2014). Using naloxone, some researchers have suggested possible interactions between histamine and opioid systems in supraspinal modulation of pain and analgesia (Tamaddonfard et al 2011;Tamaddonfard and Hamzeh-Gooshchi 2014;Hamzeh-Gooshchi et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Role of the thalamic submedius nucleus histamine H1 and H2 and opioid receptors in modulation of formalin-induced orofacial pain in rats

Erfanparast

Tamaddonfard

Taati

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Histamine and opioid systems are involved in supraspinal modulation of pain. In this study, we investigated the effects of separate and combined microinjections of agonists and antagonists of histamine H 1 and H 2 and opioid receptors into the thalamic submedius (Sm) nucleus on the formalin-induced orofacial pain. Two guide cannulas were implanted into the right and left sides of the Sm in ketamineand xylazine-anesthetized rats. Orofacial formalin pain was induced by subcutaneous injection of a diluted formalin solution (50 μl, 1.5 %) into the vibrissa pad. Face rubbing durations were recorded at 3-min blocks for 45 min. Formalin produced a biphasic pain response (first phase: 0-3 min and second phase: 15-33 min). Separate and combined microinjections of histamine H 1 and H 2 receptor agonists, 2-pyridylethylamine (2-PEA) and dimaprit, respectively, and opioid receptor agonist, morphine, attenuated the second phase of pain. The analgesic effects induced by 2-PEA, dimaprit, and morphine were blocked by prior microinjections of fexofenadine (a histamine H 1 receptor antagonist), famotidine (a histamine H 2 receptor antagonist), and naloxone (an opioid receptor antagonist), respectively. Naloxone also prevented 2-PEA-and dimaprit-induced antinociception, and the analgesic effect induced by morphine was inhibited by fexofenadine and famotidine. These results showed the involvement of histamine H 1 and H 2 and opioid receptors in the Sm modulation of orofacial pain. Opioid receptor might be involved in analgesia induced by activation of histamine H 1 and H 2 receptors and vice versa.

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Interaction between histamine and morphine at the level of the hippocampus in the formalininduced orofacial pain in rats

Cited by 23 publications

References 42 publications

Systemic synergism between codeine and morphine in three pain models in mice

Systemic synergism between codeine and morphine in three pain models in mice

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Role of the thalamic submedius nucleus histamine H1 and H2 and opioid receptors in modulation of formalin-induced orofacial pain in rats

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