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Antidepressant Actions of Histone Deacetylase Inhibitors
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Zeitschriftentitel: | The Journal of Neuroscience |
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Personen und Körperschaften: | , , , , , , , , , , , , , , , |
In: | The Journal of Neuroscience, 29, 2009, 37, S. 11451-11460 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Society for Neuroscience
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Schlagwörter: |
author_facet |
Covington, Herbert E. Maze, Ian LaPlant, Quincey C. Vialou, Vincent F. Ohnishi, Yoshinori N. Berton, Olivier Fass, Dan M. Renthal, William Rush, Augustus J. Wu, Emma Y. Ghose, Subroto Krishnan, Vaishnav Russo, Scott J. Tamminga, Carol Haggarty, Stephen J. Nestler, Eric J. Covington, Herbert E. Maze, Ian LaPlant, Quincey C. Vialou, Vincent F. Ohnishi, Yoshinori N. Berton, Olivier Fass, Dan M. Renthal, William Rush, Augustus J. Wu, Emma Y. Ghose, Subroto Krishnan, Vaishnav Russo, Scott J. Tamminga, Carol Haggarty, Stephen J. Nestler, Eric J. |
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author |
Covington, Herbert E. Maze, Ian LaPlant, Quincey C. Vialou, Vincent F. Ohnishi, Yoshinori N. Berton, Olivier Fass, Dan M. Renthal, William Rush, Augustus J. Wu, Emma Y. Ghose, Subroto Krishnan, Vaishnav Russo, Scott J. Tamminga, Carol Haggarty, Stephen J. Nestler, Eric J. |
spellingShingle |
Covington, Herbert E. Maze, Ian LaPlant, Quincey C. Vialou, Vincent F. Ohnishi, Yoshinori N. Berton, Olivier Fass, Dan M. Renthal, William Rush, Augustus J. Wu, Emma Y. Ghose, Subroto Krishnan, Vaishnav Russo, Scott J. Tamminga, Carol Haggarty, Stephen J. Nestler, Eric J. The Journal of Neuroscience Antidepressant Actions of Histone Deacetylase Inhibitors General Neuroscience |
author_sort |
covington, herbert e. |
spelling |
Covington, Herbert E. Maze, Ian LaPlant, Quincey C. Vialou, Vincent F. Ohnishi, Yoshinori N. Berton, Olivier Fass, Dan M. Renthal, William Rush, Augustus J. Wu, Emma Y. Ghose, Subroto Krishnan, Vaishnav Russo, Scott J. Tamminga, Carol Haggarty, Stephen J. Nestler, Eric J. 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.1758-09.2009 <jats:p>Persistent symptoms of depression suggest the involvement of stable molecular adaptations in brain, which may be reflected at the level of chromatin remodeling. We find that chronic social defeat stress in mice causes a transient decrease, followed by a persistent increase, in levels of acetylated histone H3 in the nucleus accumbens, an important limbic brain region. This persistent increase in H3 acetylation is associated with decreased levels of histone deacetylase 2 (HDAC2) in the nucleus accumbens. Similar effects were observed in the nucleus accumbens of depressed humans studied postmortem. These changes in H3 acetylation and HDAC2 expression mediate long-lasting positive neuronal adaptations, since infusion of HDAC inhibitors into the nucleus accumbens, which increases histone acetylation, exerts robust antidepressant-like effects in the social defeat paradigm and other behavioral assays. HDAC inhibitor [<jats:italic>N</jats:italic>-(2-aminophenyl)-4-[<jats:italic>N</jats:italic>-(pyridine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275)] infusion also reverses the effects of chronic defeat stress on global patterns of gene expression in the nucleus accumbens, as determined by microarray analysis, with striking similarities to the effects of the standard antidepressant fluoxetine. Stress-regulated genes whose expression is normalized selectively by MS-275 may provide promising targets for the future development of novel antidepressant treatments. Together, these findings provide new insight into the underlying molecular mechanisms of depression and antidepressant action, and support the antidepressant potential of HDAC inhibitors and perhaps other agents that act at the level of chromatin structure.</jats:p> Antidepressant Actions of Histone Deacetylase Inhibitors The Journal of Neuroscience |
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title |
Antidepressant Actions of Histone Deacetylase Inhibitors |
title_unstemmed |
Antidepressant Actions of Histone Deacetylase Inhibitors |
title_full |
Antidepressant Actions of Histone Deacetylase Inhibitors |
title_fullStr |
Antidepressant Actions of Histone Deacetylase Inhibitors |
title_full_unstemmed |
Antidepressant Actions of Histone Deacetylase Inhibitors |
title_short |
Antidepressant Actions of Histone Deacetylase Inhibitors |
title_sort |
antidepressant actions of histone deacetylase inhibitors |
topic |
General Neuroscience |
url |
http://dx.doi.org/10.1523/jneurosci.1758-09.2009 |
publishDate |
2009 |
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11451-11460 |
description |
<jats:p>Persistent symptoms of depression suggest the involvement of stable molecular adaptations in brain, which may be reflected at the level of chromatin remodeling. We find that chronic social defeat stress in mice causes a transient decrease, followed by a persistent increase, in levels of acetylated histone H3 in the nucleus accumbens, an important limbic brain region. This persistent increase in H3 acetylation is associated with decreased levels of histone deacetylase 2 (HDAC2) in the nucleus accumbens. Similar effects were observed in the nucleus accumbens of depressed humans studied postmortem. These changes in H3 acetylation and HDAC2 expression mediate long-lasting positive neuronal adaptations, since infusion of HDAC inhibitors into the nucleus accumbens, which increases histone acetylation, exerts robust antidepressant-like effects in the social defeat paradigm and other behavioral assays. HDAC inhibitor [<jats:italic>N</jats:italic>-(2-aminophenyl)-4-[<jats:italic>N</jats:italic>-(pyridine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275)] infusion also reverses the effects of chronic defeat stress on global patterns of gene expression in the nucleus accumbens, as determined by microarray analysis, with striking similarities to the effects of the standard antidepressant fluoxetine. Stress-regulated genes whose expression is normalized selectively by MS-275 may provide promising targets for the future development of novel antidepressant treatments. Together, these findings provide new insight into the underlying molecular mechanisms of depression and antidepressant action, and support the antidepressant potential of HDAC inhibitors and perhaps other agents that act at the level of chromatin structure.</jats:p> |
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author | Covington, Herbert E., Maze, Ian, LaPlant, Quincey C., Vialou, Vincent F., Ohnishi, Yoshinori N., Berton, Olivier, Fass, Dan M., Renthal, William, Rush, Augustus J., Wu, Emma Y., Ghose, Subroto, Krishnan, Vaishnav, Russo, Scott J., Tamminga, Carol, Haggarty, Stephen J., Nestler, Eric J. |
author_facet | Covington, Herbert E., Maze, Ian, LaPlant, Quincey C., Vialou, Vincent F., Ohnishi, Yoshinori N., Berton, Olivier, Fass, Dan M., Renthal, William, Rush, Augustus J., Wu, Emma Y., Ghose, Subroto, Krishnan, Vaishnav, Russo, Scott J., Tamminga, Carol, Haggarty, Stephen J., Nestler, Eric J., Covington, Herbert E., Maze, Ian, LaPlant, Quincey C., Vialou, Vincent F., Ohnishi, Yoshinori N., Berton, Olivier, Fass, Dan M., Renthal, William, Rush, Augustus J., Wu, Emma Y., Ghose, Subroto, Krishnan, Vaishnav, Russo, Scott J., Tamminga, Carol, Haggarty, Stephen J., Nestler, Eric J. |
author_sort | covington, herbert e. |
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description | <jats:p>Persistent symptoms of depression suggest the involvement of stable molecular adaptations in brain, which may be reflected at the level of chromatin remodeling. We find that chronic social defeat stress in mice causes a transient decrease, followed by a persistent increase, in levels of acetylated histone H3 in the nucleus accumbens, an important limbic brain region. This persistent increase in H3 acetylation is associated with decreased levels of histone deacetylase 2 (HDAC2) in the nucleus accumbens. Similar effects were observed in the nucleus accumbens of depressed humans studied postmortem. These changes in H3 acetylation and HDAC2 expression mediate long-lasting positive neuronal adaptations, since infusion of HDAC inhibitors into the nucleus accumbens, which increases histone acetylation, exerts robust antidepressant-like effects in the social defeat paradigm and other behavioral assays. HDAC inhibitor [<jats:italic>N</jats:italic>-(2-aminophenyl)-4-[<jats:italic>N</jats:italic>-(pyridine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275)] infusion also reverses the effects of chronic defeat stress on global patterns of gene expression in the nucleus accumbens, as determined by microarray analysis, with striking similarities to the effects of the standard antidepressant fluoxetine. Stress-regulated genes whose expression is normalized selectively by MS-275 may provide promising targets for the future development of novel antidepressant treatments. Together, these findings provide new insight into the underlying molecular mechanisms of depression and antidepressant action, and support the antidepressant potential of HDAC inhibitors and perhaps other agents that act at the level of chromatin structure.</jats:p> |
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spelling | Covington, Herbert E. Maze, Ian LaPlant, Quincey C. Vialou, Vincent F. Ohnishi, Yoshinori N. Berton, Olivier Fass, Dan M. Renthal, William Rush, Augustus J. Wu, Emma Y. Ghose, Subroto Krishnan, Vaishnav Russo, Scott J. Tamminga, Carol Haggarty, Stephen J. Nestler, Eric J. 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.1758-09.2009 <jats:p>Persistent symptoms of depression suggest the involvement of stable molecular adaptations in brain, which may be reflected at the level of chromatin remodeling. We find that chronic social defeat stress in mice causes a transient decrease, followed by a persistent increase, in levels of acetylated histone H3 in the nucleus accumbens, an important limbic brain region. This persistent increase in H3 acetylation is associated with decreased levels of histone deacetylase 2 (HDAC2) in the nucleus accumbens. Similar effects were observed in the nucleus accumbens of depressed humans studied postmortem. These changes in H3 acetylation and HDAC2 expression mediate long-lasting positive neuronal adaptations, since infusion of HDAC inhibitors into the nucleus accumbens, which increases histone acetylation, exerts robust antidepressant-like effects in the social defeat paradigm and other behavioral assays. HDAC inhibitor [<jats:italic>N</jats:italic>-(2-aminophenyl)-4-[<jats:italic>N</jats:italic>-(pyridine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275)] infusion also reverses the effects of chronic defeat stress on global patterns of gene expression in the nucleus accumbens, as determined by microarray analysis, with striking similarities to the effects of the standard antidepressant fluoxetine. Stress-regulated genes whose expression is normalized selectively by MS-275 may provide promising targets for the future development of novel antidepressant treatments. Together, these findings provide new insight into the underlying molecular mechanisms of depression and antidepressant action, and support the antidepressant potential of HDAC inhibitors and perhaps other agents that act at the level of chromatin structure.</jats:p> Antidepressant Actions of Histone Deacetylase Inhibitors The Journal of Neuroscience |
spellingShingle | Covington, Herbert E., Maze, Ian, LaPlant, Quincey C., Vialou, Vincent F., Ohnishi, Yoshinori N., Berton, Olivier, Fass, Dan M., Renthal, William, Rush, Augustus J., Wu, Emma Y., Ghose, Subroto, Krishnan, Vaishnav, Russo, Scott J., Tamminga, Carol, Haggarty, Stephen J., Nestler, Eric J., The Journal of Neuroscience, Antidepressant Actions of Histone Deacetylase Inhibitors, General Neuroscience |
title | Antidepressant Actions of Histone Deacetylase Inhibitors |
title_full | Antidepressant Actions of Histone Deacetylase Inhibitors |
title_fullStr | Antidepressant Actions of Histone Deacetylase Inhibitors |
title_full_unstemmed | Antidepressant Actions of Histone Deacetylase Inhibitors |
title_short | Antidepressant Actions of Histone Deacetylase Inhibitors |
title_sort | antidepressant actions of histone deacetylase inhibitors |
title_unstemmed | Antidepressant Actions of Histone Deacetylase Inhibitors |
topic | General Neuroscience |
url | http://dx.doi.org/10.1523/jneurosci.1758-09.2009 |