Involvement of galanin and galanin receptor 1 in nociceptive modulation in the central nucleus of amygdala in normal and neuropathic rats

The present study was performed to explore the role of galanin and galanin receptor 1 (GalR 1) in nociceptive modulation in the central nucleus of amygdala (CeA) in normal rats and rats with neuropathy, and the involvement of GalR 1 and PKC was also investigated. The hindpaw withdrawal latencies (HW...

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Veröffentlicht in:Scientific reports 2017-11, Vol.7 (1), p.15317-10, Article 15317
Hauptverfasser: Li, Shi-Yang, Huo, Mei-Ling, Wu, Xu-Yang, Huang, Yu-Qing, Wang, Lei, Zhang, Xin, Jiang, Yan-Mei, Zhang, Meng-Lin, Wang, Lin-Lin, Yu, Long-Chuan
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container_title Scientific reports
container_volume 7
creator Li, Shi-Yang
Huo, Mei-Ling
Wu, Xu-Yang
Huang, Yu-Qing
Wang, Lei
Zhang, Xin
Jiang, Yan-Mei
Zhang, Meng-Lin
Wang, Lin-Lin
Yu, Long-Chuan
description The present study was performed to explore the role of galanin and galanin receptor 1 (GalR 1) in nociceptive modulation in the central nucleus of amygdala (CeA) in normal rats and rats with neuropathy, and the involvement of GalR 1 and PKC was also investigated. The hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations were increased in a dose-dependent manner after intra-CeA injection of galanin in both normal rats and rats with neuropathy. The increased HWLs were significantly attenuated by intra-CeA injection of galanin receptor antagonist M40, indicating an involvement of galanin receptor in nociceptive modulation in CeA. Furthermore, intra-CeA administration of the GalR 1 agonist M 617 induced increases in HWLs in normal rats, suggesting that GalR 1 may be involved in galanin-induce antinociception in CeA. Additionally, intra-CeA injection of the PKC inhibitor inhibited galanin-induced antinociception, showing an involvement of PKC in galanin-induced antinociception in CeA of normal rats. Moreover, there was a significant increase in GalR1 content in CeA in rats with neuropathy than that in normal rats. These results illustrated that galanin induced antinociception in CeA in normal rats and rats with neuropathy, and there is an up-regulation of GalR1 expression in rats with neuropathy.
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The hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations were increased in a dose-dependent manner after intra-CeA injection of galanin in both normal rats and rats with neuropathy. The increased HWLs were significantly attenuated by intra-CeA injection of galanin receptor antagonist M40, indicating an involvement of galanin receptor in nociceptive modulation in CeA. Furthermore, intra-CeA administration of the GalR 1 agonist M 617 induced increases in HWLs in normal rats, suggesting that GalR 1 may be involved in galanin-induce antinociception in CeA. Additionally, intra-CeA injection of the PKC inhibitor inhibited galanin-induced antinociception, showing an involvement of PKC in galanin-induced antinociception in CeA of normal rats. Moreover, there was a significant increase in GalR1 content in CeA in rats with neuropathy than that in normal rats. These results illustrated that galanin induced antinociception in CeA in normal rats and rats with neuropathy, and there is an up-regulation of GalR1 expression in rats with neuropathy.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-13944-6</identifier><identifier>PMID: 29127424</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38/77 ; 631/378/2629 ; 692/617 ; 82 ; Amygdala ; Animals ; Bradykinin - analogs &amp; derivatives ; Bradykinin - pharmacology ; Central Amygdaloid Nucleus - metabolism ; Central Amygdaloid Nucleus - pathology ; Central Amygdaloid Nucleus - physiopathology ; Galanin ; Galanin - analogs &amp; derivatives ; Galanin - antagonists &amp; inhibitors ; Galanin - metabolism ; Galanin - pharmacology ; GLP-1 receptor agonists ; Humanities and Social Sciences ; Injection ; Male ; multidisciplinary ; Neuralgia - drug therapy ; Neuralgia - metabolism ; Neuralgia - pathology ; Neuralgia - physiopathology ; Neuropathy ; Nociception - drug effects ; Pain perception ; Peptide Fragments - pharmacology ; Protein kinase C ; Rats ; Rats, Sprague-Dawley ; Receptor, Galanin, Type 1 - metabolism ; Rodents ; Science ; Science (multidisciplinary)</subject><ispartof>Scientific reports, 2017-11, Vol.7 (1), p.15317-10, Article 15317</ispartof><rights>The Author(s) 2017</rights><rights>2017. 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The hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations were increased in a dose-dependent manner after intra-CeA injection of galanin in both normal rats and rats with neuropathy. The increased HWLs were significantly attenuated by intra-CeA injection of galanin receptor antagonist M40, indicating an involvement of galanin receptor in nociceptive modulation in CeA. Furthermore, intra-CeA administration of the GalR 1 agonist M 617 induced increases in HWLs in normal rats, suggesting that GalR 1 may be involved in galanin-induce antinociception in CeA. Additionally, intra-CeA injection of the PKC inhibitor inhibited galanin-induced antinociception, showing an involvement of PKC in galanin-induced antinociception in CeA of normal rats. Moreover, there was a significant increase in GalR1 content in CeA in rats with neuropathy than that in normal rats. 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The hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations were increased in a dose-dependent manner after intra-CeA injection of galanin in both normal rats and rats with neuropathy. The increased HWLs were significantly attenuated by intra-CeA injection of galanin receptor antagonist M40, indicating an involvement of galanin receptor in nociceptive modulation in CeA. Furthermore, intra-CeA administration of the GalR 1 agonist M 617 induced increases in HWLs in normal rats, suggesting that GalR 1 may be involved in galanin-induce antinociception in CeA. Additionally, intra-CeA injection of the PKC inhibitor inhibited galanin-induced antinociception, showing an involvement of PKC in galanin-induced antinociception in CeA of normal rats. Moreover, there was a significant increase in GalR1 content in CeA in rats with neuropathy than that in normal rats. These results illustrated that galanin induced antinociception in CeA in normal rats and rats with neuropathy, and there is an up-regulation of GalR1 expression in rats with neuropathy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29127424</pmid><doi>10.1038/s41598-017-13944-6</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects 38/77
631/378/2629
692/617
82
Amygdala
Animals
Bradykinin - analogs & derivatives
Bradykinin - pharmacology
Central Amygdaloid Nucleus - metabolism
Central Amygdaloid Nucleus - pathology
Central Amygdaloid Nucleus - physiopathology
Galanin
Galanin - analogs & derivatives
Galanin - antagonists & inhibitors
Galanin - metabolism
Galanin - pharmacology
GLP-1 receptor agonists
Humanities and Social Sciences
Injection
Male
multidisciplinary
Neuralgia - drug therapy
Neuralgia - metabolism
Neuralgia - pathology
Neuralgia - physiopathology
Neuropathy
Nociception - drug effects
Pain perception
Peptide Fragments - pharmacology
Protein kinase C
Rats
Rats, Sprague-Dawley
Receptor, Galanin, Type 1 - metabolism
Rodents
Science
Science (multidisciplinary)
title Involvement of galanin and galanin receptor 1 in nociceptive modulation in the central nucleus of amygdala in normal and neuropathic rats
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