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

Authors:
Ramanan N, Shen Y, Sarsfield S, Lemberger T, Sch├╝tz G, Linden DJ, Ginty DD
Associated Labs:
Ginty Lab (Johns Hopkins University and School of Medicine)
Nat Neurosci. 2005 Jun . 8(6):759-67.
PMID: 15880109
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.

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