Resveratrol attenuates N-methyl-D-aspartate receptor-mediated activation in substantia gelatinosa neurons of trigeminal subnucleus caudalis in mice
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초록
The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives orofacial nociceptive information from primary afferent neurons and transmits this information to higher brain centers. Resveratrol (3, 5, 4′-trihydroxystilbene) is a polyphenolic compound found in various plant species and have been reported to have various biological activities, including analgesic effects. Although many studies have investigated the mechanism of action of resveratrol in terms of its antinociceptive effect, limited research has been conducted on the effects of resveratrol on SG neurons involved in orofacial pain transmission, especially to understand its relevance to glutamate receptors. To address this research gap, the present study investigated the effect of resveratrol on glutamate receptor activity in SG neurons using the whole-cell patch-clamp technique. The results showed that resveratrol significantly inhibited glutamate-mediated inward currents in SG neurons. Notably, there were no changes in α-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid- or kainic acid-mediated inward currents in the presence of resveratrol, although N-methyl-D-aspartate (NMDA)-mediated inward currents were markedly suppressed. Taken together, these results suggest that resveratrol may be involved in orofacial pain transmission in SG neurons of the Vc by inhibiting the activity of NMDA receptors, among ionotropic glutamate receptors.
Abstract
The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives orofacial nociceptive information from primary afferent neurons and transmits this information to higher brain centers. Resveratrol (3, 5, 4′-trihydroxystilbene) is a polyphenolic compound found in various plant species and have been reported to have various biological activities, including analgesic effects. Although many studies have investigated the mechanism of action of resveratrol in terms of its antinociceptive effect, limited research has been conducted on the effects of resveratrol on SG neurons involved in orofacial pain transmission, especially to understand its relevance to glutamate receptors. To address this research gap, the present study investigated the effect of resveratrol on glutamate receptor activity in SG neurons using the whole-cell patch-clamp technique. The results showed that resveratrol significantly inhibited glutamate-mediated inward currents in SG neurons. Notably, there were no changes in α-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid- or kainic acid-mediated inward currents in the presence of resveratrol, although N-methyl-D-aspartate (NMDA)-mediated inward currents were markedly suppressed. Taken together, these results suggest that resveratrol may be involved in orofacial pain transmission in SG neurons of the Vc by inhibiting the activity of NMDA receptors, among ionotropic glutamate receptors.
참고문헌 (42)
- Sessle BJ, "Acute and chronic craniofacial pain : brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates", Crit Rev Oral Biol Med, 11, pp.57~91 (2000)[DOI]
- Cervero F, "The substantia gelatinosa of the spinal cord : a critical review", Brain, 103, pp.717~772 (1980)[DOI]
- Todd AJ, "Neuronal circuitry for pain processing in the dorsal horn", Nat Rev Neurosci, 11, pp.823~836 (2010)[DOI]
- Fundytus ME, "Glutamate receptors and nociception : implications for the drug treatment of pain", CNS Drugs, 15, pp.29~58 (2001)[DOI]
- Mennerick S, "Encyclopedia of life sciences", pp.1~8 (2012), John Wiley & Sons
- Peltoniemi MA, "Ketamine : a review of clinical pharmacokinetics and pharmacodynamics in anesthesia and pain therapy", Clin Pharmacokinet, 55, pp.1059~1077 (2016)[DOI]
- Pickering G, "Memantine for the treatment of general neuropathic pain : a narrative review", Fundam Clin Pharmacol, 32, pp.4~13 (2018)[DOI]
- Podkowa K, "The NMDA receptor antagonists memantine and ketamine as anti-migraine agents", Naunyn Schmiedebergs Arch Pharmacol, 396, pp.1371~1398 (2023)[DOI]
- Frémont L, "Biological effects of resveratrol", Life Sci, 66, pp.663~673 (2000)[DOI]
- Pervaiz S, "Resveratrol : from grapevines to mammalian biology", FASEB J, 17, pp.1975~1985 (2003)[DOI]
- Bazzo KO, "Evidence for the analgesic activity of resveratrol in acute models of nociception in mice", J Nat Prod, 76, pp.13~21 (2013)[DOI]
- Granados-Soto V, "The peripheral antinociceptive effect of resveratrol is associated with activation of potassium channels", Neuropharmacology, 43, pp.917~923 (2002)[DOI]
- Pan X, "Resveratrolinduced antinociception is involved in calcium channels and calcium", caffeine-sensitive pools, 2017, pp.8, 9399~9409
- Pham-Marcou TA, "Antinociceptive effect of resveratrol in carrageenan-evoked hyperalgesia in rats : prolonged effect related to COX-2 expression impairment", Pain, 140, pp.274~283 (2008)[DOI]
- Sekiguchi K, "Resveratrol attenuates inflammation-induced hyperexcitability of trigeminal spinal nucleus caudalis neurons associated with hyperalgesia in rats", Mol Pain, 12 (2016)[DOI]
- Sharma S, "Effect of resveratrol, a polyphenolic phytoalexin, on thermal hyperalgesia in a mouse model of diabetic neuropathic pain", Fundam Clin Pharmacol, 21, pp.89~94 (2007)[DOI]
- Singh AK, "Anti-nociceptive effect of resveratrol during inflammatory hyperalgesia via differential regulation of pro-inflammatory mediators", Phytother Res, 30, pp.1164~1171 (2016)[DOI]
- Tao L, "Resveratrol attenuates neuropathic pain through balancing pro-inflammatory and anti-inflammatory cytokines release in mice", Int Immunopharmacol, 34, pp.165~172 (2016)[DOI]
- Wang LL, "Resveratrol attenuates inflammatory hyperalgesia by inhibiting glial activation in mice spinal cords", Mol Med Rep, 13, pp.4051~4057 (2016)[DOI]
- Wang W, "The analgesic effect of transresveratrol is regulated by calcium channels in the hippocampus of mice", Metab Brain Dis, 32, pp.1311~1321 (2017)[DOI]
- Yang YJ, "Resveratrol suppresses glial activation and alleviates trigeminal neuralgia via activation of AMPK", J Neuroinflammation, 13, pp.84~ (2016)[DOI]
- Yin Q, "Resveratrol facilitates pain attenuation in a rat model of neuropathic pain through the activation of spinal Sirt1", Reg Anesth Pain Med, 38, pp.93~99 (2013)[DOI]
- Yu L, "Modulation of TRP channels by resveratrol and other stilbenoids", Mol Pain, 9, pp.3~ (2013)[DOI]
- Jang SH, "Resveratrol activates GABAA and", or glycine receptors on substantia gelatinosa neurons of the subnucleus caudalis in mice, 2022, pp.36, 5788~5792
- Phuong Thao Thi Nguyen, "Inhibitory actions of borneol on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice", The Korean Journal of Physiology & Pharmacology, 24(5), pp.433~440 (2020), 대한약리학회[DOI]
- Meldrum BS, "Glutamate as a neurotransmitter in the brain : review of physiology and pathology", J Nutr, 130(4S Suppl), pp.1007S~1015S (2000)[DOI]
- Ferraguti F, "Metabotropic glutamate receptors", Cell Tissue Res, 326, pp.483~504 (2006)[DOI]
- Takehana S, "The dietary constituent resveratrol suppresses nociceptive neurotransmission via the NMDA receptor", Mol Pain, 13 (2017)[DOI]
- Hsieh CP, "Differential inhibitory effects of resveratrol on excitotoxicity and synaptic plasticity : involvement of NMDA receptor subtypes", Nutr Neurosci, 24, pp.443~458 (2021)[DOI]
- Gao ZB, "Inhibition of excitatory synaptic transmission by trans-resveratrol in rat hippocampus", Brain Res, 1111, pp.41~47 (2006)[DOI]
- Zhang H, "Resveratrol attenuates early pyramidal neuron excitability impairment and death in acute rat hippocampal slices caused by oxygen-glucose deprivation", Exp Neurol, 212, pp.44~52 (2008)[DOI]
- Wang YJ, "Distinct effects of resveratrol on seizures and hyperexcitability induced by NMDA and 4-aminopyridine", Nutr Neurosci, 22, pp.867~876 (2019)[DOI]
- Li Z, "Resveratrol protects CA1neurons against focal cerebral ischemic reperfusioninduced damage via the ERK-CREB signaling pathway in rats", Pharmacol Biochem Behav (2016)[DOI]
- Han YS, "Neuroprotective effects of resveratrol against beta-amyloid-induced neurotoxicity in rat hippocampal neurons : involvement of protein kinase C", Br J Pharmacol, 141, pp.997~1005 (2004)[DOI]
- Saleh MC, "Resveratrol preconditioning induces cellular stress proteins and is mediated via NMDA and estrogen receptors", Neuroscience, 166, pp.445~454 (2010)[DOI]
- Quincozes-Santos A, "Oxidative stress mediated by NMDA, AMPA", KA channels in acute hippocampal slices : neuroprotective effect of resveratrol, 2014, pp.28, 544~551
- Karthick C, "Intrahippocampal administration of Ibotenic acid induced cholinergic dysfunction via NR2A", NR2B expression : implications of resveratrol against Alzheimer disease pathophysiology, 2016, pp.9, 28~
- Sánchez-Melgar A, "Resveratrol differently modulates group I metabotropic glutamate receptors depending on age in SAMP8 mice", ACS Chem Neurosci, 11, pp.1770~1780 (2020)[DOI]
- Lee BH, "Resveratrol inhibits glycine receptor-mediated ion currents", Biol Pharm Bull, 37, pp.576~580 (2014)[DOI]
- Groundwater PW, "The differential effects of resveratrol and trans-ε-viniferin on the GABA-induced current in GABAA receptor subtypes expressed in Xenopus laevis oocytes", J Pharm Pharm Sci, 18, pp.328~338 (2015)[DOI]
- Lee BH, "Resveratrol enhances 5-hydroxytryptamine type 3A receptor-mediated ion currents : the role of arginine 222residue in pre-transmembrane domain I", Biol Pharm Bull, 34, pp.523~527 (2011)[DOI]
- Oliveira CDC, "Evidence for the involvement of opioid and cannabinoid systems in the peripheral antinociception mediated by resveratrol", Toxicol Appl Pharmacol, 369, pp.30~38 (2019)[DOI]
