The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice

Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ i...
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Autor*in:	Clark W. Bird [verfasserIn] Carlos F. Valenzuela [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	allosteric apoptosis cortex development electrophysiology ethanol

Übergeordnetes Werk:	In: Neuropsychopharmacology Reports - Wiley, 2018, 43(2023), 1, Seite 77-84
Übergeordnetes Werk:	volume:43 ; year:2023 ; number:1 ; pages:77-84

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/npr2.12306

Katalog-ID:	DOAJ08790165X

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245	1	4	\|a The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
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520			\|a Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development.
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spelling	10.1002/npr2.12306 doi (DE-627)DOAJ08790165X (DE-599)DOAJfa4e9877013f42f09ef55207d0bbe74b DE-627 ger DE-627 rakwb eng RM1-950 RC321-571 Clark W. Bird verfasserin aut The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development. allosteric apoptosis cortex development electrophysiology ethanol Therapeutics. Pharmacology Neurosciences. Biological psychiatry. Neuropsychiatry Carlos F. Valenzuela verfasserin aut In Neuropsychopharmacology Reports Wiley, 2018 43(2023), 1, Seite 77-84 (DE-627)1030679681 (DE-600)2942336-3 2574173X nnns volume:43 year:2023 number:1 pages:77-84 https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/article/fa4e9877013f42f09ef55207d0bbe74b kostenfrei https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/toc/2574-173X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_65 GBV_ILN_69 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 43 2023 1 77-84
allfields_unstemmed	10.1002/npr2.12306 doi (DE-627)DOAJ08790165X (DE-599)DOAJfa4e9877013f42f09ef55207d0bbe74b DE-627 ger DE-627 rakwb eng RM1-950 RC321-571 Clark W. Bird verfasserin aut The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development. allosteric apoptosis cortex development electrophysiology ethanol Therapeutics. Pharmacology Neurosciences. Biological psychiatry. Neuropsychiatry Carlos F. Valenzuela verfasserin aut In Neuropsychopharmacology Reports Wiley, 2018 43(2023), 1, Seite 77-84 (DE-627)1030679681 (DE-600)2942336-3 2574173X nnns volume:43 year:2023 number:1 pages:77-84 https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/article/fa4e9877013f42f09ef55207d0bbe74b kostenfrei https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/toc/2574-173X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_65 GBV_ILN_69 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 43 2023 1 77-84
allfieldsGer	10.1002/npr2.12306 doi (DE-627)DOAJ08790165X (DE-599)DOAJfa4e9877013f42f09ef55207d0bbe74b DE-627 ger DE-627 rakwb eng RM1-950 RC321-571 Clark W. Bird verfasserin aut The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development. allosteric apoptosis cortex development electrophysiology ethanol Therapeutics. Pharmacology Neurosciences. Biological psychiatry. Neuropsychiatry Carlos F. Valenzuela verfasserin aut In Neuropsychopharmacology Reports Wiley, 2018 43(2023), 1, Seite 77-84 (DE-627)1030679681 (DE-600)2942336-3 2574173X nnns volume:43 year:2023 number:1 pages:77-84 https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/article/fa4e9877013f42f09ef55207d0bbe74b kostenfrei https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/toc/2574-173X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_65 GBV_ILN_69 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 43 2023 1 77-84
allfieldsSound	10.1002/npr2.12306 doi (DE-627)DOAJ08790165X (DE-599)DOAJfa4e9877013f42f09ef55207d0bbe74b DE-627 ger DE-627 rakwb eng RM1-950 RC321-571 Clark W. Bird verfasserin aut The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development. allosteric apoptosis cortex development electrophysiology ethanol Therapeutics. Pharmacology Neurosciences. Biological psychiatry. Neuropsychiatry Carlos F. Valenzuela verfasserin aut In Neuropsychopharmacology Reports Wiley, 2018 43(2023), 1, Seite 77-84 (DE-627)1030679681 (DE-600)2942336-3 2574173X nnns volume:43 year:2023 number:1 pages:77-84 https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/article/fa4e9877013f42f09ef55207d0bbe74b kostenfrei https://doi.org/10.1002/npr2.12306 kostenfrei https://doaj.org/toc/2574-173X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_65 GBV_ILN_69 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 43 2023 1 77-84
language	English
source	In Neuropsychopharmacology Reports 43(2023), 1, Seite 77-84 volume:43 year:2023 number:1 pages:77-84
sourceStr	In Neuropsychopharmacology Reports 43(2023), 1, Seite 77-84 volume:43 year:2023 number:1 pages:77-84
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	allosteric apoptosis cortex development electrophysiology ethanol Therapeutics. Pharmacology Neurosciences. Biological psychiatry. Neuropsychiatry
isfreeaccess_bool	true
container_title	Neuropsychopharmacology Reports
authorswithroles_txt_mv	Clark W. Bird @@aut@@ Carlos F. Valenzuela @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	1030679681
id	DOAJ08790165X
language_de	englisch
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callnumber-first	R - Medicine
author	Clark W. Bird
spellingShingle	Clark W. Bird misc RM1-950 misc RC321-571 misc allosteric misc apoptosis misc cortex misc development misc electrophysiology misc ethanol misc Therapeutics. Pharmacology misc Neurosciences. Biological psychiatry. Neuropsychiatry The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
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topic_title	RM1-950 RC321-571 The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice allosteric apoptosis cortex development electrophysiology ethanol
topic	misc RM1-950 misc RC321-571 misc allosteric misc apoptosis misc cortex misc development misc electrophysiology misc ethanol misc Therapeutics. Pharmacology misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_unstemmed	misc RM1-950 misc RC321-571 misc allosteric misc apoptosis misc cortex misc development misc electrophysiology misc ethanol misc Therapeutics. Pharmacology misc Neurosciences. Biological psychiatry. Neuropsychiatry
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title	The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
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title_full	The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
author_sort	Clark W. Bird
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author_browse	Clark W. Bird Carlos F. Valenzuela
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title_sort	positive allosteric modulator of nmda receptors, gne‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
callnumber	RM1-950
title_auth	The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
abstract	Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development.
abstractGer	Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development.
abstract_unstemmed	Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development.
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title_short	The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice
url	https://doi.org/10.1002/npr2.12306 https://doaj.org/article/fa4e9877013f42f09ef55207d0bbe74b https://doaj.org/toc/2574-173X
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Bird</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Binge‐like exposure to ethanol during the brain growth spurt triggers apoptotic neurodegeneration in multiple brain regions, including the retrosplenial cortex, a brain region that is part of the hippocampal‐diencephalic‐cingulate memory network. This is mediated, in part, by reduced Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors followed by a decrease in the activation of pro‐survival genes. Here, we tested whether a positive allosteric modulator of NMDA receptors could counteract the inhibitory effect of ethanol on developing retrosplenial cortex pyramidal neurons. We used patch‐clamp electrophysiological techniques in acute slices from postnatal day 6–8 mice to test the effect of the positive allosteric modulator GNE‐9278 on ethanol‐induced inhibition of NMDA receptor function. GNE‐9278 dose‐dependently increased the amplitude, decay time, and total charge of NMDA excitatory postsynaptic currents. At a concentration of 5 μmol L−1, GNE‐9278 significantly reduced the 90 mmol L−1 ethanol‐induced inhibition of NMDA excitatory postsynaptic current amplitude, decay time, and total charge. Current‐clamp experiments showed that 5 μmol L−1 GNE‐9278 ameliorated the 90 mmol L−1 ethanol‐induced inhibition of synaptically‐evoked action potential firing and compound excitatory postsynaptic potential amplitude. These findings indicate that positive allosteric modulators mitigate ethanol‐induced hypofunction of NMDA receptors in developing cerebral cortex neurons, an effect that could ameliorate its pro‐apoptotic effects during the late stages of fetal development.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">allosteric</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">apoptosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cortex</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">development</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">electrophysiology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ethanol</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Therapeutics. 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The positive allosteric modulator of NMDA receptors, GNE‐9278, blocks the ethanol‐induced decrease of excitability in developing retrosplenial cortex neurons from mice

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