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Inhibition by 2-methoxy-4-ethylphenol of Ca2+ influx through acquired and native N-methyl-D-aspartate-receptor channels.
J Pharmacol Sci. 2010; 112(3):273-81.JP

Abstract

Pharmacological properties were evaluated for the antidiarrheic wood creosote ingredient 2-methoxy-4-ethylphenol (2M4EP), which was shown to be protective against neurotoxicity of N-methyl-D-aspartate (NMDA), to modulate Ca(2+) influx across acquired and native NMDA receptor (NMDAR) channels. NMDA markedly increased intracellular free Ca(2+) levels in HEK293 cells transfected with the expression vector of either NR2A or NR2B subunit together with the essential NR1 subunit vector. Further addition of dizocilpine inhibited the increase by NMDA in intracellular Ca(2+) levels in both types of acquired NMDAR channels, while 2M4EP and the NR2B-subunit-selective antagonist ifenprodil were more effective in inhibiting the increase by NMDA in HEK293 cells expressing NR1/NR2B subunits than in those with NR1/NR2A subunits. 2M4EP significantly prevented the increased intracellular Ca(2+) levels by NMDA in cultured rat hippocampal neurons. Brief exposure to NMDA led to a drastic decrease in cellular viability 24 h later in cultured hippocampal neurons, while 2M4EP significantly prevented the loss of cellular vitality by NMDA. Similarly, 2M4EP more efficiently protected HEK293 cells with NR1/NR2B subunits than those with NR1/NR2A subunits. These results suggest that 2M4EP may protect neurons from excitotoxicity through inhibition of Ca(2+) influx across NMDAR channels composed of NR1/NR2B, rather than NR1/NR2A, subunits.

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Authors+Show Affiliations

Fukumori R
Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School of Natural Science and Technology, Kanazawa, Ishikawa 920-1192, Japan.
Nakamichi N
No affiliation info available
Takarada T
No affiliation info available
Kambe Y
No affiliation info available
Matsushima N
No affiliation info available
Moriguchi N
No affiliation info available
Yoneda Y
No affiliation info available

MeSH

AnimalsCalciumCell LineCell SurvivalCells, CulturedGuaiacolHumansN-MethylaspartateRatsRats, WistarReceptors, N-Methyl-D-Aspartate

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20168047

Citation

Fukumori, Ryo, et al. "Inhibition By 2-methoxy-4-ethylphenol of Ca2+ Influx Through Acquired and Native N-methyl-D-aspartate-receptor Channels." Journal of Pharmacological Sciences, vol. 112, no. 3, 2010, pp. 273-81.
Fukumori R, Nakamichi N, Takarada T, et al. Inhibition by 2-methoxy-4-ethylphenol of Ca2+ influx through acquired and native N-methyl-D-aspartate-receptor channels. J Pharmacol Sci. 2010;112(3):273-81.
Fukumori, R., Nakamichi, N., Takarada, T., Kambe, Y., Matsushima, N., Moriguchi, N., & Yoneda, Y. (2010). Inhibition by 2-methoxy-4-ethylphenol of Ca2+ influx through acquired and native N-methyl-D-aspartate-receptor channels. Journal of Pharmacological Sciences, 112(3), 273-81.
Fukumori R, et al. Inhibition By 2-methoxy-4-ethylphenol of Ca2+ Influx Through Acquired and Native N-methyl-D-aspartate-receptor Channels. J Pharmacol Sci. 2010;112(3):273-81. PubMed PMID: 20168047.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition by 2-methoxy-4-ethylphenol of Ca2+ influx through acquired and native N-methyl-D-aspartate-receptor channels. AU - Fukumori,Ryo, AU - Nakamichi,Noritaka, AU - Takarada,Takeshi, AU - Kambe,Yuki, AU - Matsushima,Nobuyuki, AU - Moriguchi,Nobuaki, AU - Yoneda,Yukio, Y1 - 2010/02/18/ PY - 2010/2/20/entrez PY - 2010/2/20/pubmed PY - 2010/10/30/medline SP - 273 EP - 81 JF - Journal of pharmacological sciences JO - J Pharmacol Sci VL - 112 IS - 3 N2 - Pharmacological properties were evaluated for the antidiarrheic wood creosote ingredient 2-methoxy-4-ethylphenol (2M4EP), which was shown to be protective against neurotoxicity of N-methyl-D-aspartate (NMDA), to modulate Ca(2+) influx across acquired and native NMDA receptor (NMDAR) channels. NMDA markedly increased intracellular free Ca(2+) levels in HEK293 cells transfected with the expression vector of either NR2A or NR2B subunit together with the essential NR1 subunit vector. Further addition of dizocilpine inhibited the increase by NMDA in intracellular Ca(2+) levels in both types of acquired NMDAR channels, while 2M4EP and the NR2B-subunit-selective antagonist ifenprodil were more effective in inhibiting the increase by NMDA in HEK293 cells expressing NR1/NR2B subunits than in those with NR1/NR2A subunits. 2M4EP significantly prevented the increased intracellular Ca(2+) levels by NMDA in cultured rat hippocampal neurons. Brief exposure to NMDA led to a drastic decrease in cellular viability 24 h later in cultured hippocampal neurons, while 2M4EP significantly prevented the loss of cellular vitality by NMDA. Similarly, 2M4EP more efficiently protected HEK293 cells with NR1/NR2B subunits than those with NR1/NR2A subunits. These results suggest that 2M4EP may protect neurons from excitotoxicity through inhibition of Ca(2+) influx across NMDAR channels composed of NR1/NR2B, rather than NR1/NR2A, subunits. SN - 1347-8648 UR - https://www.unboundmedicine.com/medline/citation/20168047/Inhibition_by_2_methoxy_4_ethylphenol_of_Ca2+_influx_through_acquired_and_native_N_methyl_D_aspartate_receptor_channels_ L2 - https://linkinghub.elsevier.com/retrieve/pii/JST.JSTAGE/jphs/09294FP DB - PRIME DP - Unbound Medicine ER -
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