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21	MSK1 regulates homeostatic and experience-dependent synaptic plasticity 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. January 2012 (has links) No / 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. 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
22	The mechanism mediating fast neurotransmitter release at the calyx of Held synapse / Der Mechanismus der schnellen Neurotransmitterfreisetzung an der Held Wadel, Kristian 20 October 2008 (has links) No description available. 570 Biowissenschaften Biologie Elektrophysiologie Exozytose Exzitatorischer Postsynaptischer Strom Held'sche Calyx Hirnstamm Kalzium Kalziumkanäle Kinetik Modelle Neurotransmitter Patch-Clamp Techniken Photolyse Präsynaptische Nervenendigung Ratten Synapsen Synaptische Übertragung Synaptische Vesikel Tiere Animals Brain Stem Calcium Calcium Channels Calyx of Held Electrophysiology Excitatory Postsynaptic Currents Exocytosis Kinetics Models Neurotransmitters Patch-Clamp Techniques Photolysis Presynaptic Terminals Rats Synapses Synaptic Transmission Synaptic Vesicles 42.12 42.15 42.17

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MSK1 regulates homeostatic and experience-dependent synaptic plasticity

The mechanism mediating fast neurotransmitter release at the calyx of Held synapse / Der Mechanismus der schnellen Neurotransmitterfreisetzung an der Held