NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture
We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death thro...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Choi, So-Young [verfasserIn] Hwang, Jung Jin [verfasserIn] Koh, Jae-Young [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|
| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2004 |
|---|
| Schlagwörter: |
|---|
| Umfang: |
Online-Ressource |
|---|
| Reproduktion: |
2003 ; Blackwell Publishing Journal Backfiles 1879-2005 |
|---|---|
| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 88(2004), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:88 ; year:2004 ; number:3 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1046/j.1471-4159.2003.02187.x |
|---|
| Katalog-ID: |
NLEJ24312449X |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ24312449X | ||
| 003 | DE-627 | ||
| 005 | 20210707172821.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 120427s2004 xx |||||o 00| ||und c | ||
| 024 | 7 | |a 10.1046/j.1471-4159.2003.02187.x |2 doi | |
| 035 | |a (DE-627)NLEJ24312449X | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 100 | 1 | |a Choi, So-Young |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| 264 | 1 | |a Oxford, UK |b Blackwell Science Ltd |c 2004 | |
| 300 | |a Online-Ressource | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. | ||
| 533 | |d 2003 |f Blackwell Publishing Journal Backfiles 1879-2005 |7 |2003|||||||||| | ||
| 650 | 4 | |a Egr-1 | |
| 700 | 1 | |a Hwang, Jung Jin |e verfasserin |4 aut | |
| 700 | 1 | |a Koh, Jae-Young |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i In |t Journal of neurochemistry |d Oxford : Wiley-Blackwell, 1956 |g 88(2004), 3, Seite 0 |h Online-Ressource |w (DE-627)NLEJ243927584 |w (DE-600)2020528-4 |x 1471-4159 |7 nnns |
| 773 | 1 | 8 | |g volume:88 |g year:2004 |g number:3 |g pages:0 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x |q text/html |x Verlag |z Deutschlandweit zugänglich |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a ZDB-1-DJB | ||
| 912 | |a GBV_NL_ARTICLE | ||
| 951 | |a AR | ||
| 952 | |d 88 |j 2004 |e 3 |h 0 | ||
| author_variant |
s y c syc j j h jj jjh j y k jyk |
|---|---|
| matchkey_str |
article:14714159:2004----::ranutoadmaeetreednnuoadahyertoh |
| hierarchy_sort_str |
2004 |
| publishDate |
2004 |
| allfields |
10.1046/j.1471-4159.2003.02187.x doi (DE-627)NLEJ24312449X DE-627 ger DE-627 rakwb Choi, So-Young verfasserin aut NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Egr-1 Hwang, Jung Jin verfasserin aut Koh, Jae-Young verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 3 0 |
| spelling |
10.1046/j.1471-4159.2003.02187.x doi (DE-627)NLEJ24312449X DE-627 ger DE-627 rakwb Choi, So-Young verfasserin aut NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Egr-1 Hwang, Jung Jin verfasserin aut Koh, Jae-Young verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 3 0 |
| allfields_unstemmed |
10.1046/j.1471-4159.2003.02187.x doi (DE-627)NLEJ24312449X DE-627 ger DE-627 rakwb Choi, So-Young verfasserin aut NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Egr-1 Hwang, Jung Jin verfasserin aut Koh, Jae-Young verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 3 0 |
| allfieldsGer |
10.1046/j.1471-4159.2003.02187.x doi (DE-627)NLEJ24312449X DE-627 ger DE-627 rakwb Choi, So-Young verfasserin aut NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Egr-1 Hwang, Jung Jin verfasserin aut Koh, Jae-Young verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 3 0 |
| allfieldsSound |
10.1046/j.1471-4159.2003.02187.x doi (DE-627)NLEJ24312449X DE-627 ger DE-627 rakwb Choi, So-Young verfasserin aut NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Egr-1 Hwang, Jung Jin verfasserin aut Koh, Jae-Young verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 3 0 |
| source |
In Journal of neurochemistry 88(2004), 3, Seite 0 volume:88 year:2004 number:3 pages:0 |
| sourceStr |
In Journal of neurochemistry 88(2004), 3, Seite 0 volume:88 year:2004 number:3 pages:0 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
Egr-1 |
| isfreeaccess_bool |
false |
| container_title |
Journal of neurochemistry |
| authorswithroles_txt_mv |
Choi, So-Young @@aut@@ Hwang, Jung Jin @@aut@@ Koh, Jae-Young @@aut@@ |
| publishDateDaySort_date |
2004-01-01T00:00:00Z |
| hierarchy_top_id |
NLEJ243927584 |
| id |
NLEJ24312449X |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ24312449X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707172821.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2004 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.1471-4159.2003.02187.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ24312449X</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Choi, So-Young</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2004</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2003</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2003||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Egr-1</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hwang, Jung Jin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Koh, Jae-Young</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of neurochemistry</subfield><subfield code="d">Oxford : Wiley-Blackwell, 1956</subfield><subfield code="g">88(2004), 3, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243927584</subfield><subfield code="w">(DE-600)2020528-4</subfield><subfield code="x">1471-4159</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:88</subfield><subfield code="g">year:2004</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">88</subfield><subfield code="j">2004</subfield><subfield code="e">3</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| series2 |
Blackwell Publishing Journal Backfiles 1879-2005 |
| author |
Choi, So-Young |
| spellingShingle |
Choi, So-Young misc Egr-1 NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| authorStr |
Choi, So-Young |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ243927584 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| author_role |
aut aut aut |
| collection |
NL |
| publishPlace |
Oxford, UK |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1471-4159 |
| topic_title |
NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture Egr-1 |
| publisher |
Blackwell Science Ltd |
| publisherStr |
Blackwell Science Ltd |
| topic |
misc Egr-1 |
| topic_unstemmed |
misc Egr-1 |
| topic_browse |
misc Egr-1 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| hierarchy_parent_title |
Journal of neurochemistry |
| hierarchy_parent_id |
NLEJ243927584 |
| hierarchy_top_title |
Journal of neurochemistry |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ243927584 (DE-600)2020528-4 |
| title |
NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| ctrlnum |
(DE-627)NLEJ24312449X |
| title_full |
NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| author_sort |
Choi, So-Young |
| journal |
Journal of neurochemistry |
| journalStr |
Journal of neurochemistry |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
2004 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| author_browse |
Choi, So-Young Hwang, Jung Jin Koh, Jae-Young |
| container_volume |
88 |
| physical |
Online-Ressource |
| format_se |
Elektronische Aufsätze |
| author-letter |
Choi, So-Young |
| doi_str_mv |
10.1046/j.1471-4159.2003.02187.x |
| author2-role |
verfasserin |
| title_sort |
nr2a induction and nmda receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| title_auth |
NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| abstract |
We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. |
| abstractGer |
We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. |
| abstract_unstemmed |
We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death. |
| collection_details |
GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE |
| container_issue |
3 |
| title_short |
NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture |
| url |
http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x |
| remote_bool |
true |
| author2 |
Hwang, Jung Jin Koh, Jae-Young |
| author2Str |
Hwang, Jung Jin Koh, Jae-Young |
| ppnlink |
NLEJ243927584 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| doi_str |
10.1046/j.1471-4159.2003.02187.x |
| up_date |
2024-07-06T04:22:26.774Z |
| _version_ |
1803802112714342400 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ24312449X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707172821.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2004 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.1471-4159.2003.02187.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ24312449X</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Choi, So-Young</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">NR2A induction and NMDA receptor-dependent neuronal death by neurotrophin-4/5 in cortical cell culture</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2004</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">We have previously shown that prolonged exposure to neurotrophins induces oxidative neuronal death. In the present study, we further examined the cascades involved in neurotrophin-4/5 (NT-4/5)-induced neuronal death. Exposure of mature cortical cultures for 48 h to NT-4/5 induced neuronal death through TrkB activation. The NT-4/5-induced neuronal death was largely attenuated by addition of MK-801, indicating a critical role for NMDA receptors. Western blots revealed the induction of NR2A by NT-4/5. In addition, levels of phospho-NR2A and 2B increased, suggesting the upregulation of the NMDA receptor function. Whereas glutamate levels in the media changed little, levels of d-serine and l-glycine, co-agonists at NMDA receptors, increased significantly following NT-4/5 treatment. Exposure to NT-4/5 resulted in the activation of Src and extracellular signal-regulated kinase-1/2 (Erk-1/2). Their inhibitors blocked NR2A induction and phosphorylation as well as neuronal death induced by NT-4/5. In addition, Egr-1 was induced in an Src- and Erk-1/2-dependent manner. Anti-sense oligodeoxynucleotides to egr-1 attenuated NR2A induction as well as neuronal death. Although induction of NADPH oxidase and neuronal nitric oxide synthase (nNOS) contributes to NT-4/5-induced neuronal death, inhibition of their activity did not reduce NR2A induction. Conversely, blockade of NMDA receptors did not attenuate induction of NADPH oxidase or nNOS. These results indicate that two events are largely independent of each other. Our results demonstrate that the signaling cascade of TrkB leads to increase in NMDA receptor activity. Whereas this cascade may play an important role in the modulation of NMDA receptors in physiologic conditions, in the context of TrkB overactivation, it may contribute to neuronal death.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2003</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2003||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Egr-1</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hwang, Jung Jin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Koh, Jae-Young</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of neurochemistry</subfield><subfield code="d">Oxford : Wiley-Blackwell, 1956</subfield><subfield code="g">88(2004), 3, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243927584</subfield><subfield code="w">(DE-600)2020528-4</subfield><subfield code="x">1471-4159</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:88</subfield><subfield code="g">year:2004</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.1471-4159.2003.02187.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">88</subfield><subfield code="j">2004</subfield><subfield code="e">3</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.400324 |