Interaction between the dopaminergic and opioidergic systems in dorsal hippocampus in modulation of formalin-induced orofacial pain in rats

Reisi, Zahra; Haghparast, Amir; Pahlevani, Pouyan; Shamsizadeh, Ali; Haghparast, Abbas

doi:10.1016/j.pbb.2014.06.015

Cited by 14 publications

(9 citation statements)

References 45 publications

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“…Our results are consistent with co-release of these neurotransmitters in these regions. Along with the existing literature (Sulzer et al 2016, Kirkpatrick et al 2015, Reisi et al 2014, our results suggest that pain modulation during sensory/emotional pain conditions activates both dopamine and opioid receptors. Our results support the existing literature, in that we found the striatum to have the highest activation in both dopaminergic and opioidergic meta-analyses.…”

Section: Discussionsupporting

confidence: 89%

Pain-related opioidergic and dopaminergic neurotransmission: Dual Meta-Analyses of PET Radioligand Studies

Guerra

Spadoni

Mitchell³

et al. 2020

Preprint

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Molecular mechanisms of the interaction between pain and reward associated with pain relief processes in the human brain are still incompletely understood. This is partially due to the invasive nature of the available techniques to visualize and measure metabolic activity. Positron Emission Tomography (PET) radioligand studies using radioactive substances are still the only available modality to date that allows for the investigation of the molecular mechanisms in the human brain. For pain and reward studies, the most commonly studied PET radiotracers are [11C]-carfentanil (CFN) and [11C]- or [18F]-diprenorphine (DPN), which bind to opioid receptors, and [11C]-raclopride (RAC) and [18F]-fallypride (FAL) tracers, which bind to dopamine receptors. The current meta-analysis looks at 15 pain-related studies using opioid radioligands and 8 studies using dopamine radioligands in an effort to consolidate the available data into the most likely activated regions. Our primary goal was to identify regions of shared opioid/dopamine neurotransmission during pain-related experiences. SDM analysis of previously published voxel coordinate data showed that opioidergic activations were strongest in the bilateral caudate, thalamus, right putamen, cingulate gyrus, midbrain, inferior frontal gyrus, and left superior temporal gyrus. The dopaminergic studies showed that the bilateral caudate, thalamus, right putamen, cingulate gyrus, and left putamen had the highest activations. We were able to see a clear overlap between opioid and dopamine activations in a majority of the regions during pain-related processing, though there were some unique areas of dopaminergic activation such as the left putamen. Regions unique to opioidergic activation include the midbrain, inferior frontal gyrus, and left superior temporal gyrus. By investigating the regions of dopaminergic and opioidergic activation, we can potentially provide more targeted treatment to these sets of receptors in patients with pain conditions. These findings could eventually assist in the development of more targeted medication in order to help treat pain conditions and simultaneously prevent physical dependency.

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Section: Discussionsupporting

confidence: 89%

Pain-related opioidergic and dopaminergic neurotransmission: Dual Meta-Analyses of PET Radioligand Studies

Guerra

Spadoni

Mitchell³

et al. 2020

Preprint

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“…† p<0.05 as compared with 2-PEA (2 μg/site) and morphine (2 μg/site)-treated groups. ‡ p<0.05 as compared with dimaprit (2 μg/site) and morphine (2 μg/site)-treated groups hippocampus, and dentate gyrus produced analgesic effects in the orofacial formalin pain in rats (Rosenfeld and Stocco 1981;Duale et al 2007;Khalilzadeh et al 2010;Tamaddonfard et al 2011;Reisi et al 2014). In the thalamic parafascicular nucleus, microinjection of morphine attenuated the affective reaction to noxious stimulation in rats (Munn et al 2009).…”

Section: Discussionmentioning

confidence: 94%

“…The first phase is associated to direct stimulation of nociceptors, whereas the second phase reflects integration between nociceptors and spinal and brainstem signaling (Raboisson and Dallel 2004). Face rubbing with the ipsilateral forepaw due to formalin injection into the vibrissa pad has been mentioned as a specific nociceptive response in rats and mice (Donatti et al 2014;Reisi et al 2014;Miranda et al 2013;Tamaddonfard et al 2011;Luccarini et al 2003).…”

Section: Discussionmentioning

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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“…Haloperidol antagonized the antinociceptive effect of propranolol-morphine only in the first phase of the formalin test. Similarly, sulpiride another D 2 receptor antagonist reversed the antinociceptive effects of morphine only in the first phase of formalin-induced orofacial pain in rats ( Reisi et al, 2014 ). The failure of haloperidol to attenuate the antinociceptive effect of propranolol-morphine in the second phase of formalin test is difficult to explain.…”

Section: Discussionmentioning

confidence: 99%

Potentiation of Morphine-Induced Antinociception by Propranolol: The Involvement of Dopamine and GABA Systems

Afify

Andijani

2017

Front. Pharmacol.

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Tolerance to the analgesic effect of morphine is a major clinical problem which can be managed by co-administration of another drug. This study investigated the ability of propranolol to potentiate the antinociceptive action of morphine and the possible mechanisms underlying this effect. Antinociception was assessed in three nociceptive tests (thermal, hot plate), (visceral, acetic acid), and (inflammatory, formalin test) in mice and quantified by measuring the percent maximum possible effect, the percent inhibition of acetic acid-evoked writhing response, and the area under the curve values of number of flinches for treated mice, respectively. The study revealed that propranolol (0.25–20 mg/Kg, IP) administration did not produce analgesia in mice. However, 10 mg/Kg propranolol, enhanced the antinociceptive effect of sub-analgesic doses of morphine (0.2, 1, and 2 mg/Kg, IP) in the three nociceptive tests. It also shifted the dose response curve of morphine to the left. The combined effect of propranolol and morphine was attenuated by haloperidol (D2 receptor antagonist, 1.5 mg/Kg, IP), and bicuculline (GABAA receptor antagonist, 2 mg/Kg, IP). Repeated daily administration of propranolol (10 mg/Kg, IP) did not alter the nociceptive responses in the three pain tests, but it significantly potentiated morphine-induced antinociception in the hot plate, acetic acid-evoked writhing, and in the second phase of formalin tests. Together, the data suggest that a cross-talk exists between the opioidergic and adrenergic systems and implicate dopamine and GABA systems in this synergistic effect of morphine-propranolol combination. Propranolol may serve as an adjuvant therapy to potentiate the effect of opioid analgesics.

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Interaction between the dopaminergic and opioidergic systems in dorsal hippocampus in modulation of formalin-induced orofacial pain in rats

Cited by 14 publications

References 45 publications

Pain-related opioidergic and dopaminergic neurotransmission: Dual Meta-Analyses of PET Radioligand Studies

Pain-related opioidergic and dopaminergic neurotransmission: Dual Meta-Analyses of PET Radioligand Studies

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

Potentiation of Morphine-Induced Antinociception by Propranolol: The Involvement of Dopamine and GABA Systems

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