دورية أكاديمية
The interaction between alpha 7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-alpha represents a new antinociceptive signaling pathway in mice
العنوان: | The interaction between alpha 7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-alpha represents a new antinociceptive signaling pathway in mice |
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المؤلفون: | Donvito, Giulia, Toma, Wisam, Rahimpour, Elnaz, Jackson, Asti, Meade, Julie A., Alsharari, Shakir, Kulkarni, Abhijit R., Carroll, F. Ivy, Lichtman, Aron H., Papke, Roger L, Thakur, Ganesh A., Damaj, M. Imad |
المساهمون: | Uludağ Üniversitesi/Tıp Fakültesi/Deney Hayvanları Yetiştirme ve Araştırma Merkezi., Bağdaş, Deniz, 15062425700 |
بيانات النشر: | Elsevier |
سنة النشر: | 2017 |
المجموعة: | Açık Erişim@BUU (Bursa Uludağ Üniversitesi) |
مصطلحات موضوعية: | Neurosciences & neurology, Alpha7, Mice, Nicotinic acetylcholine receptors, Nuclear peroxisome proliferator-activated receptor type-α, Palmitoylethanolamide, Tonic pain, Positive allosteric modulator, Neuropathic pain, Inflammatory pain, G-proteins, Agonist, Models, Pnu-120596, Mechanism, Gat107, Target, Alpha7 nicotinic acetylcholine receptor, Animals, Azabicyclo compounds, Benzamides, Bridged bicyclo compounds, Cannabinoid receptor antagonists, Ethanolamines, Furans, Male, inbred ICR, Nicotinic antagonists, Nociception, Oxazoles |
الوصف: | Recently, alpha 7 nicotinic acetylcholine receptors (nAChRs), primarily activated by binding of orthosteric agonists, represent a target for anti-inflammatory and analgesic drug development. These receptors may also be modulated by positive allosteric modulators (PAMs), ago-allosteric ligands (ago-PAMs), and alpha 7-silent agonists. Activation of 00 nAChRs has been reported to increase the brain levels of endogenous ligands for nuclear peroxisome proliferator-activated receptors type-alpha (PPAR-alpha), palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), in a Ca2+-dependent manner. Here, we investigated potential crosstalk between alpha 7 nAChR and PPAR-alpha, using the formalin test, a mouse model of tonic pain. Using pharmacological and genetic approaches, we found that PNU282987, a full alpha 7 agonist, attenuated formalin-induced nociceptive behavior in alpha 7 -dependent manner. Interestingly, the selective PPAR-alpha antagonist GW6471 blocked the antinociceptive effects of PNU282987, but did not alter the antinociceptive responses evoked by the alpha 7 nAChR PAM PNU120596, ago-PAM GAT107, and silent agonist NS6740. Moreover, GW6471 administered systemically or spinally, but not via the intraplantar surface of the formalin-injected paw blocked PNU282987-induced antinociception. Conversely, exogenous administration of the naturally occurring PPAR-alpha agonist PEA potentiated the antinociceptive effects of PNU282987. In contrast, the cannabinoid 031 antagonist rimonabant and the CB2 antagonist SR144528 failed to reverse the antinociceptive effects of PNU282987. These findings suggest that PPAR-alpha plays a key role in a putative antinociceptive alpha 7 nicotinic signaling pathway. ; United States Department of Health & Human Services National Institutes of Health (NIH) - USA - GM57481 - R01 CA206028 ; United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Cancer Institute (NCI) - R01CA206028 ; United States Department of Health & Human ... |
نوع الوثيقة: | article in journal/newspaper |
وصف الملف: | application/pdf |
اللغة: | English |
تدمد: | 0014-4886 1090-2430 |
العلاقة: | Makale - Uluslararası Hakemli Dergi; Experimental Neurology; Yurt dışı; Donvito, G. vd. (2017). ''The interaction between alpha 7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-alpha represents a new antinociceptive signaling pathway in mice''. Experimental Neurology, 295, 194-201.; https://doi.org/10.1016/j.expneurol.2017.06.014Test; https://www.sciencedirect.com/science/article/pii/S001448861730153XTest; http://hdl.handle.net/11452/29379Test; 000406820900019; 2-s2.0-85020773276; 194; 201; 295 |
DOI: | 10.1016/j.expneurol.2017.06.014 |
الإتاحة: | https://doi.org/10.1016/j.expneurol.2017.06.014Test http://hdl.handle.net/11452/29379Test https://www.sciencedirect.com/science/article/pii/S001448861730153XTest |
حقوق: | info:eu-repo/semantics/openAccess ; Atıf Gayri Ticari Türetilemez 4.0 Uluslararası ; http://creativecommons.org/licenses/by-nc-nd/4.0Test/ |
رقم الانضمام: | edsbas.B0156E00 |
قاعدة البيانات: | BASE |
تدمد: | 00144886 10902430 |
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DOI: | 10.1016/j.expneurol.2017.06.014 |