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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, experimental evidence indicates that synaptic plasticity is metabolically demanding as well. As synaptic plasticity is crucial for learning, we examine how these metabolic costs enter in learning. We find that when synaptic plasticity rules are naively implemented, training neural networks requires extremely large amounts of energy when storing many patterns. We propose that this is avoided by precisely balancing labile forms of synaptic plasticity with more stable forms. This algorithm, termed synaptic caching, boosts energy efficiency manifold and can be used with any plasticity rule, including back-propagation. Our results yield a novel interpretation of the multiple forms of neural synaptic plasticity observed experimentally, including synaptic tagging and capture phenomena. Furthermore our results are relevant for energy efficient neuromorphic designs.
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The development of novel synaptic device architectures with a high order of synaptic plasticity can provide a breakthrough toward neuromorphic computing. Herein, through the thermal oxidation of two-d...
Dendritic spines, the carriers of long-term memory, occupy a small fraction of cortical space, and yet they are the major consumers of brain metabolic energy. What fraction of this energy goes for syn...
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 ...
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...
The project is targeting cognitive impairment, one of the main health problems of patients with RAS pathway disorders. The aim of this study is to translate findings of animal studies to h...
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...
Depression is the leading cause of disability globally (1, 2). One-third to one-half of patients suffering from major depressive disorder (MDD) do not achieve remission even after multiple...
This study aims to measure synaptic density in the brains (including in ventral striatum [VS] and medial prefrontal cortex [mPFC]) of abstinent subjects with Cocaine Use Disorder (CUD) or ...
An important mechanism responsible for clinical recovery after neurological damage of different types is synaptic plasticity. Nervous tissue can enhance or de-energize inter-neuronal trans...
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.
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.
Electric power supply devices which convert biological energy, such as chemical energy of metabolism or mechanical energy of periodic movements, into electrical energy.