mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway

Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-A...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Chen, Hwei-Hsien [verfasserIn] Liao, Pei-Fei Chan, Ming-Huan

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Schlagwörter:	NMDA Receptor Hippocampal Slice NMDA Receptor Antagonist NMDA Receptor Activation Ifenprodil

Anmerkung:	© Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: Journal of biomedical science - London : BioMed Central, 1994, 18(2011), 1 vom: 22. Feb.
Übergeordnetes Werk:	volume:18 ; year:2011 ; number:1 ; day:22 ; month:02

Links:	Volltext

DOI / URN:	10.1186/1423-0127-18-19

Katalog-ID:	SPR028488644

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520			\|a Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists.
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allfields	10.1186/1423-0127-18-19 doi (DE-627)SPR028488644 (SPR)1423-0127-18-19-e DE-627 ger DE-627 rakwb eng Chen, Hwei-Hsien verfasserin aut mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. NMDA Receptor (dpeaa)DE-He213 Hippocampal Slice (dpeaa)DE-He213 NMDA Receptor Antagonist (dpeaa)DE-He213 NMDA Receptor Activation (dpeaa)DE-He213 Ifenprodil (dpeaa)DE-He213 Liao, Pei-Fei aut Chan, Ming-Huan aut Enthalten in Journal of biomedical science London : BioMed Central, 1994 18(2011), 1 vom: 22. Feb. (DE-627)300593724 (DE-600)1482918-6 1423-0127 nnns volume:18 year:2011 number:1 day:22 month:02 https://dx.doi.org/10.1186/1423-0127-18-19 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2011 1 22 02
spelling	10.1186/1423-0127-18-19 doi (DE-627)SPR028488644 (SPR)1423-0127-18-19-e DE-627 ger DE-627 rakwb eng Chen, Hwei-Hsien verfasserin aut mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. NMDA Receptor (dpeaa)DE-He213 Hippocampal Slice (dpeaa)DE-He213 NMDA Receptor Antagonist (dpeaa)DE-He213 NMDA Receptor Activation (dpeaa)DE-He213 Ifenprodil (dpeaa)DE-He213 Liao, Pei-Fei aut Chan, Ming-Huan aut Enthalten in Journal of biomedical science London : BioMed Central, 1994 18(2011), 1 vom: 22. Feb. (DE-627)300593724 (DE-600)1482918-6 1423-0127 nnns volume:18 year:2011 number:1 day:22 month:02 https://dx.doi.org/10.1186/1423-0127-18-19 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2011 1 22 02
allfields_unstemmed	10.1186/1423-0127-18-19 doi (DE-627)SPR028488644 (SPR)1423-0127-18-19-e DE-627 ger DE-627 rakwb eng Chen, Hwei-Hsien verfasserin aut mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. NMDA Receptor (dpeaa)DE-He213 Hippocampal Slice (dpeaa)DE-He213 NMDA Receptor Antagonist (dpeaa)DE-He213 NMDA Receptor Activation (dpeaa)DE-He213 Ifenprodil (dpeaa)DE-He213 Liao, Pei-Fei aut Chan, Ming-Huan aut Enthalten in Journal of biomedical science London : BioMed Central, 1994 18(2011), 1 vom: 22. Feb. (DE-627)300593724 (DE-600)1482918-6 1423-0127 nnns volume:18 year:2011 number:1 day:22 month:02 https://dx.doi.org/10.1186/1423-0127-18-19 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2011 1 22 02
allfieldsGer	10.1186/1423-0127-18-19 doi (DE-627)SPR028488644 (SPR)1423-0127-18-19-e DE-627 ger DE-627 rakwb eng Chen, Hwei-Hsien verfasserin aut mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. NMDA Receptor (dpeaa)DE-He213 Hippocampal Slice (dpeaa)DE-He213 NMDA Receptor Antagonist (dpeaa)DE-He213 NMDA Receptor Activation (dpeaa)DE-He213 Ifenprodil (dpeaa)DE-He213 Liao, Pei-Fei aut Chan, Ming-Huan aut Enthalten in Journal of biomedical science London : BioMed Central, 1994 18(2011), 1 vom: 22. Feb. (DE-627)300593724 (DE-600)1482918-6 1423-0127 nnns volume:18 year:2011 number:1 day:22 month:02 https://dx.doi.org/10.1186/1423-0127-18-19 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2011 1 22 02
allfieldsSound	10.1186/1423-0127-18-19 doi (DE-627)SPR028488644 (SPR)1423-0127-18-19-e DE-627 ger DE-627 rakwb eng Chen, Hwei-Hsien verfasserin aut mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. NMDA Receptor (dpeaa)DE-He213 Hippocampal Slice (dpeaa)DE-He213 NMDA Receptor Antagonist (dpeaa)DE-He213 NMDA Receptor Activation (dpeaa)DE-He213 Ifenprodil (dpeaa)DE-He213 Liao, Pei-Fei aut Chan, Ming-Huan aut Enthalten in Journal of biomedical science London : BioMed Central, 1994 18(2011), 1 vom: 22. Feb. (DE-627)300593724 (DE-600)1482918-6 1423-0127 nnns volume:18 year:2011 number:1 day:22 month:02 https://dx.doi.org/10.1186/1423-0127-18-19 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2011 1 22 02
language	English
source	Enthalten in Journal of biomedical science 18(2011), 1 vom: 22. Feb. volume:18 year:2011 number:1 day:22 month:02
sourceStr	Enthalten in Journal of biomedical science 18(2011), 1 vom: 22. Feb. volume:18 year:2011 number:1 day:22 month:02
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	NMDA Receptor Hippocampal Slice NMDA Receptor Antagonist NMDA Receptor Activation Ifenprodil
isfreeaccess_bool	true
container_title	Journal of biomedical science
authorswithroles_txt_mv	Chen, Hwei-Hsien @@aut@@ Liao, Pei-Fei @@aut@@ Chan, Ming-Huan @@aut@@
publishDateDaySort_date	2011-02-22T00:00:00Z
hierarchy_top_id	300593724
id	SPR028488644
language_de	englisch
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. 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author	Chen, Hwei-Hsien
spellingShingle	Chen, Hwei-Hsien misc NMDA Receptor misc Hippocampal Slice misc NMDA Receptor Antagonist misc NMDA Receptor Activation misc Ifenprodil mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway
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topic_title	mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway NMDA Receptor (dpeaa)DE-He213 Hippocampal Slice (dpeaa)DE-He213 NMDA Receptor Antagonist (dpeaa)DE-He213 NMDA Receptor Activation (dpeaa)DE-He213 Ifenprodil (dpeaa)DE-He213
topic	misc NMDA Receptor misc Hippocampal Slice misc NMDA Receptor Antagonist misc NMDA Receptor Activation misc Ifenprodil
topic_unstemmed	misc NMDA Receptor misc Hippocampal Slice misc NMDA Receptor Antagonist misc NMDA Receptor Activation misc Ifenprodil
topic_browse	misc NMDA Receptor misc Hippocampal Slice misc NMDA Receptor Antagonist misc NMDA Receptor Activation misc Ifenprodil
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title	mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway
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title_full	mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway
author_sort	Chen, Hwei-Hsien
journal	Journal of biomedical science
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author_browse	Chen, Hwei-Hsien Liao, Pei-Fei Chan, Ming-Huan
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author-letter	Chen, Hwei-Hsien
doi_str_mv	10.1186/1423-0127-18-19
title_sort	mglur5 positive modulators both potentiate activation and restore inhibition in nmda receptors by pkc dependent pathway
title_auth	mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway
abstract	Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background In order to understand the interaction between the metabotropic glutamate subtype 5 (mGluR5) and N-methyl-D-aspartate (NMDA) receptors, the influence of mGluR5 positive modulators in the inhibition of NMDA receptors by the noncompetitive antagonist ketamine, the competitive antagonist D-APV and the selective NR2B inhibitor ifenprodil was investigated. Methods This study used the multi-electrode dish (MED) system to observe field potentials in hippocampal slices of mice. Results Data showed that the mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), as well as the positive allosteric modulators 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) and 3,3'-difluorobenzaldazine (DFB) alone did not alter the basal field potentials, but enhanced the amplitude of field potentials induced by NMDA. The inhibitory action of ketamine on NMDA-induced response was reversed by CHPG, DFB, and CDPPB, whereas the blockade of NMDA receptor by D-APV was restored by CHPG and CDPPB, but not by DFB. Alternatively, activation of NMDA receptors prior to the application of mGluR5 modulators, CHPG was able to enhance NMDA-induced field potentials and reverse the suppressive effect of ketamine and D-APV, but not ifenprodil. In addition, chelerythrine chloride (CTC), a protein kinase C (PKC) inhibitor, blocked the regulation of mGluR5 positive modulators in enhancing NMDA receptor activation and recovering NMDA receptor inhibition. The PKC activator (PMA) mimicked the effects of mGluR5 positive modulators on enhancing NMDA receptor activation and reversing NMDA antagonist-evoked NMDA receptor suppression. Conclusion Our results demonstrate that the PKC-dependent pathway may be involved in the positive modulation of mGluR5 resulting in potentiating NMDA receptor activation and reversing NMDA receptor suppression induced by NMDA antagonists. © Chen et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway
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mGluR5 positive modulators both potentiate activation and restore inhibition in NMDA receptors by PKC dependent pathway

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