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Nat Neurosci. 2005 Jun;8(6):759-67. Epub 2005 May 8.

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

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  • 1Department of Neuroscience, 725 North Wolfe Street, Preclinical Teaching Building Room 1015, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

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.

PMID:
15880109
[PubMed - indexed for MEDLINE]
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