2005
DOI: 10.1038/nn1462
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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-respo… Show more

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Cited by 199 publications
(236 citation statements)
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“…79 In contrast to the initial report of SRF deletion in CNS neurons, 76 an independent group using the same Camk2a Cre driver did not report any defects in the neuronal cyto-architecture and migration or postnatal lethality. 33 Instead, they showed decreases in SRF-dependent immediate-early gene expression (eg, Fos) after exposure of mice to a new environment and impaired long-term potentiation of cortical neurons suggestive of synaptic pathology. Of note, SRF expression and binding activity to a CArG box have been shown to increase in a rat model of epilepsy, 81 a disease of neuronal hyper-excitability and neuronal plasticity, which affects up to 2% of the world population.…”
Section: Srf and Nervous System Disease Central Nervous Systemmentioning
confidence: 98%
See 1 more Smart Citation
“…79 In contrast to the initial report of SRF deletion in CNS neurons, 76 an independent group using the same Camk2a Cre driver did not report any defects in the neuronal cyto-architecture and migration or postnatal lethality. 33 Instead, they showed decreases in SRF-dependent immediate-early gene expression (eg, Fos) after exposure of mice to a new environment and impaired long-term potentiation of cortical neurons suggestive of synaptic pathology. Of note, SRF expression and binding activity to a CArG box have been shown to increase in a rat model of epilepsy, 81 a disease of neuronal hyper-excitability and neuronal plasticity, which affects up to 2% of the world population.…”
Section: Srf and Nervous System Disease Central Nervous Systemmentioning
confidence: 98%
“…Studies using this floxed Srf mouse showed no measurable SRF entity after Cre-mediated excision. 32,33 In this review, I highlight the salient pathologies associated with the genetic loss of SRF in individual organ systems of the mouse. An up-to-date list of cell-specific SRF knockouts is provided in Table 1, and the readers are encouraged to consult the original literature for some of the nuances associated with each knockout.…”
mentioning
confidence: 99%
“…The activity of other transcription factors, such as SRF, c-fos, egr1 or NF-κβ (Albensi and Mattson, 2000;Izquierdo and Cammarota, 2004;Ramanan et al, 2005;Tischmeyer and Grimm, 1999) can also promote de novo gene expression and support long-lasting changes in synaptic plasticity. The expression of some of these TFs, such as c-fos, egr1 or C/EBPβ, is itself induced during LTP formation and their activity can trigger a second wave of gene expression that may also be important for LTP consolidation.…”
Section: Accepted Manuscriptmentioning
confidence: 99%
“…Aberrance of adaptive responses such as long-term memory or late-phase synaptic plasticity has indeed been the hallmark of several genetically engineered mouse mutants in which the expression or the function of key transcription factors have been altered (2,3). Thus it appears that the supply of neuronal proteins must be tightly matched to the cellular demand at any given time, to maintain proper neuronal circuit function.…”
mentioning
confidence: 99%