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Synaptic plasticity, with its two most studied forms, long-term potentiation (LTP) and long-term depression (LTD), is the cellular mechanism underlying learning and memory. Although it has been known for two decades that bidirectional synaptic plasticity necessitates a corresponding bidirectional regulation of calcineurin activity, the underlying molecular mechanism remains elusive. Using organotypic hippocampal slice cultures, we show here that phosphorylation of the endogenous regulator-of-calcineurin (RCAN1) by GSK3β underlies calcineurin activation and is a necessary event for LTD induction, while phosphorylation of RCAN1 at a PKA site blocks calcineurin activity, thereby allowing LTP induction. Our results provide a new mechanism for the regulation of calcineurin in bidirectional synaptic plasticity and establish RCAN1 as a "switch" for bidirectional synaptic plasticity.
This article was published in the following journal.
Name: Current biology : CB
Many aspects of the brain's design can be understood as the result of evolutionary drive towards metabolic efficiency. In addition to the energetic costs of neural computation and transmission, experi...
Transient receptor potential (TRP) proteins form Ca2+-permeable, nonselective cation channels, but their role in neuronal Ca2+ homeostasis is elusive. In the present paper, we show that TRPC channels ...
Phosphorylation regulates glutamate receptor trafficking. The cytosolic C-terminal domains of both NMDA receptors (NMDARs) and AMPA receptors (AMPARs) have distinct motifs, which are substrates for se...
Persistent changes that occur in brain circuits are classically thought to be mediated by long-term modifications in synaptic efficacy. Yet, many studies have shown that voltage-gated ion channels loc...
NMDA receptor (NMDAR) subunit composition plays a pivotal role in synaptic plasticity at excitatory synapses. Still, the mechanisms responsible for the synaptic retention of NMDARs following induction...
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The hypothesis underlying this proposal is that deficits of synaptic plasticity underlie the slow-wave activity (SWA) abnormalities observed n major depressive disorder (MDD), and that man...
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A neuronal protein consisting of three PDZ DOMAINS, an SH3 DOMAIN, and a C-terminal guanylate kinase-like region (see MAGUK PROTEINS). It localizes to the POST-SYNAPTIC DENSITY and associates with the cytoplasmic tail of NMDA RECEPTORS and SHAKER POTASSIUM CHANNELS, playing a critical role in NMDA receptor-mediated SYNAPTIC PLASTICITY.
Myelin proteins that are expressed as three isoforms: Nogo-A, Nogo-B, and Nogo-C. These share a C-terminal reticulon homology domain (RHD), consisting of two hydrophobic membrane domains flanking a 66 amino acid (Nogo-66) hydrophilic region. A long transmembrane region allows conformations that either span the entire membrane or fold into a hairpin conformation. Nogo inhibits NEURITE outgrowth and modulates wiring and the restriction of SYNAPTIC PLASTICITY in the adult central nervous system. It also regulates neurite fasciculation, branching, and extension in the developing nervous system.
Cytoskeleton specialization at the cytoplasmic side of postsynaptic membrane in SYNAPSES. It is involved in neuronal signaling and NEURONAL PLASTICITY and comprised of GLUTAMATE RECEPTORS; scaffolding molecules (e.g., PSD95, PSD93), and other proteins (e.g., CaCMKII).
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
Serine/threonine protein kinase responsible for various SKELETAL MUSCLE functions; HEART CONDUCTION SYSTEM activity; calcium HOMEOSTASIS; calcium uptake by SARCOPLASMIC RETICULUM and SYNAPTIC PLASTICITY. It is encoded by the DMPK gene and its abnormal EXPANDED TRINUCLEOTIDE REPEAT of CTG in the 3'-UTR is associated with MYOTONIC DYSTROPHY 1.
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