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SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability.

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Title: SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability.
Authors: Ramanan, Narendrakumar, Ying Shen, Sarsfield, Sarah, Lemberger, Thomas, Schütz, Günther, Linden, David J., Ginty, David D.
Source: Nature Neuroscience. Jun2005, Vol. 8 Issue 6, p759-767. 9p.
Subjects: Gene expression, Synapses, Neuroplasticity, Nervous system, Neurons, Brain, Mammals
Abstract: Synaptic activity-dependent gene expression is critical for certain forms of neuronal plasticity and survival in the mammalian nervous system, yet the mechanisms by which coordinated regulation of activity-induced genes supports neuronal function is unclear. Here, we show that deletion of serum response factor (SRF) in specific neuronal populations in adult mice results in profound deficits in activity-dependent immediate early gene expression, but components of upstream signaling pathways and cyclic AMP-response element binding protein (CREB)-dependent transactivation remain intact. Moreover, SRF-deficient CA1 pyramidal neurons show attenuation of long-term synaptic potentiation, a model for neuronal information storage. Furthermore, in contrast to the massive neurodegeneration seen in adult mice lacking CREB family members, SRF-deficient adult neurons show normal morphologies and basal excitatory synaptic transmission. These findings indicate that the transcriptional events underlying neuronal survival and plasticity are dissociable and that SRF plays a prominent role in use-dependent modification of synaptic strength in the adult brain. [ABSTRACT FROM AUTHOR]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability.
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  Data: <searchLink fieldCode="AR" term="%22Ramanan%2C+Narendrakumar%22">Ramanan, Narendrakumar</searchLink><br /><searchLink fieldCode="AR" term="%22Ying+Shen%22">Ying Shen</searchLink><br /><searchLink fieldCode="AR" term="%22Sarsfield%2C+Sarah%22">Sarsfield, Sarah</searchLink><br /><searchLink fieldCode="AR" term="%22Lemberger%2C+Thomas%22">Lemberger, Thomas</searchLink><br /><searchLink fieldCode="AR" term="%22Schütz%2C+Günther%22">Schütz, Günther</searchLink><br /><searchLink fieldCode="AR" term="%22Linden%2C+David+J%2E%22">Linden, David J.</searchLink><br /><searchLink fieldCode="AR" term="%22Ginty%2C+David+D%2E%22">Ginty, David D.</searchLink>
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  Data: Synaptic activity-dependent gene expression is critical for certain forms of neuronal plasticity and survival in the mammalian nervous system, yet the mechanisms by which coordinated regulation of activity-induced genes supports neuronal function is unclear. Here, we show that deletion of serum response factor (SRF) in specific neuronal populations in adult mice results in profound deficits in activity-dependent immediate early gene expression, but components of upstream signaling pathways and cyclic AMP-response element binding protein (CREB)-dependent transactivation remain intact. Moreover, SRF-deficient CA1 pyramidal neurons show attenuation of long-term synaptic potentiation, a model for neuronal information storage. Furthermore, in contrast to the massive neurodegeneration seen in adult mice lacking CREB family members, SRF-deficient adult neurons show normal morphologies and basal excitatory synaptic transmission. These findings indicate that the transcriptional events underlying neuronal survival and plasticity are dissociable and that SRF plays a prominent role in use-dependent modification of synaptic strength in the adult brain. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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              Text: Jun2005
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