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

Narendrakumar Ramanan, Ying Shen, Sarah Sarsfield, Thomas Lemberger, Günther Schütz, David J. Linden, David D. Ginty

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)759-767
Number of pages9
JournalNature neuroscience
Volume8
Issue number6
DOIs
StatePublished - Jun 2005

ASJC Scopus subject areas

  • Neuroscience(all)

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