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    MSK1 regulates homeostatic and experience-dependent synaptic plasticity

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    Publication date
    2012
    Author
    Corrêa, Sonia A.L.
    Hunter, C.J.
    Palygin, O.
    Wauters, S.C.
    Martin, K.J.
    McKenzie, C.
    McKelvey, K.
    Morris, R.G.
    Pankratov, Y.
    Arthur, J.S.
    Frenguelli, B.G.
    Show allShow less
    Keyword
    Analysis of Variance
    ; Animals
    ; Brain-derived neurotrophic factor
    ; Cells
    ; Cytoskeletal proteins
    ; Dendritic spines
    ; Environment
    ; Enzyme inhibitors
    ; Excitatory postsynaptic potentials
    ; Female
    ; Gene expression regulation
    ; Green fluorescent proteins
    ; Hippocampus
    ; Homeostasis
    ; Male
    Mice; Inbred C57BL
    ; Transgenic
    ; Nerve tissue proteins
    ; Neuronal plasticity
    ; Neurons
    ; Patch-clamp techniques
    ; Point mutation
    ; Receptors; AMPA
    ; Ribosomal protein S6 kinases
    ; Signal transduction
    ; Sodium channel blockers
    ; Synapses
    ; Tetrodotoxin
    ; Time factors
    ; REF 2014
    Show allShow less
    Peer-Reviewed
    Yes
    
    Metadata
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    Abstract
    The ability of neurons to modulate synaptic strength underpins synaptic plasticity, learning and memory, and adaptation to sensory experience. Despite the importance of synaptic adaptation in directing, reinforcing, and revising the behavioral response to environmental influences, the cellular and molecular mechanisms underlying synaptic adaptation are far from clear. Brain-derived neurotrophic factor (BDNF) is a prime initiator of structural and functional synaptic adaptation. However, the signaling cascade activated by BDNF to initiate these adaptive changes has not been elucidated. We have previously shown that BDNF activates mitogen- and stress-activated kinase 1 (MSK1), which regulates gene transcription via the phosphorylation of both CREB and histone H3. Using mice with a kinase-dead knock-in mutation of MSK1, we now show that MSK1 is necessary for the upregulation of synaptic strength in response to environmental enrichment in vivo. Furthermore, neurons from MSK1 kinase-dead mice failed to show scaling of synaptic transmission in response to activity deprivation in vitro, a deficit that could be rescued by reintroduction of wild-type MSK1. We also show that MSK1 forms part of a BDNF- and MAPK-dependent signaling cascade required for homeostatic synaptic scaling, which likely resides in the ability of MSK1 to regulate cell surface GluA1 expression via the induction of Arc/Arg3.1. These results demonstrate that MSK1 is an integral part of a signaling pathway that underlies the adaptive response to synaptic and environmental experience. MSK1 may thus act as a key homeostat in the activity- and experience-dependent regulation of synaptic strength.
    URI
    http://hdl.handle.net/10454/5942
    Version
    No full-text in the repository
    Citation
    Correa SA, Hunter CJ, Palygin O et al (2012) MSK1 regulates homeostatic and experience-dependent synaptic plasticity. Journal of Neuroscience. 32(38): 13039-13051.
    Link to publisher’s version
    http://dx.doi.org/10.1523/JNEUROSCI.0930-12.2012
    Type
    Article
    Collections
    Life Sciences Publications

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