We propose a scalable synaptic circuit realizing spike timing dependent plasticity (STDP)-compatible with randomly spiking neurons. The feasible working of the circuit was examined by circuit simulation using the BSIM 4.6.0 model. A distinguishable feature of the circuit is the use of floating-gate integrators that provide the compact implementation of biologically plausible relaxation time scale. This relaxation occurs on the basis of charge tunneling that mainly relies upon area-independent tunnel barrier properties (e.g. barrier width and height) rather than capacitance. The circuit simulations feature (i) weight-dependent STDP that spontaneously limits the synaptic weight growth, (ii) competitive synaptic adaptation within both unsupervised and supervised frameworks with randomly spiking neurons. The estimated power consumption is merely 34 pW, perhaps meeting one of the most crucial principles (power-efficiency) of neuromorphic engineering. Finally, a means of fine-tuning the STDP behavior is provided.
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http://dx.doi.org/10.1038/s41598-017-17889-8 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Group of Microbial Motility, Department of Biological Science, Division of Natural Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan.
Age-dependent sensory impairment, memory loss, and cognitive decline are generally attributed to neuron loss, synaptic dysfunction, and decreased neuronal activities over time. Concurrently, increased neuronal activity is reported in humans and other organisms during aging. However, it is unclear whether neuronal hyperactivity is the cause of cognitive impairment or a compensatory mechanism of circuit dysfunction.
View Article and Find Full Text PDFFront Neural Circuits
December 2024
Department of Cellular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan.
Our brain adapts to the environment by optimizing its function through experience-dependent cortical plasticity. This plasticity is transiently enhanced during a developmental stage, known as the "critical period," and subsequently maintained at lower levels throughout adulthood. Thus, understanding the mechanism underlying critical period plasticity is crucial for improving brain adaptability across the lifespan.
View Article and Find Full Text PDFJ Neurosci
December 2024
Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA
Excitatory synapses and the actin-rich dendritic spines on which they reside are indispensable for information processing and storage in the brain. In the adult hippocampus, excitatory synapses must balance plasticity and stability to support learning and memory. However, the mechanisms governing this balance remain poorly understood.
View Article and Find Full Text PDFNeurosci Res
December 2024
Laboratory of Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya University, Nagoya, Japan; Laboratory of Neural Information Processing, Institute for Advanced Research, Nagoya University, Nagoya, Japan; PRESTO/CREST, Japan Science and Technology Agency, Saitama, Japan. Electronic address:
Despite the crucial role of synaptic connections and neural activity in the development and organization of cortical circuits, the mechanisms underlying the formation of functional synaptic connections in the developing human cerebral cortex remain unclear. We investigated the development of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated synaptic transmission using human cortical organoids (hCOs) derived from induced pluripotent stem cells. Two-photon Ca⁺ imaging revealed an increase in the frequency and amplitude of spontaneous activity in hCOs on day 80 compared to day 50.
View Article and Find Full Text PDFCurr Opin Neurobiol
December 2024
Department of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045, USA. Electronic address:
GABAergic synaptic inhibition controls circuit function by regulating neuronal plasticity, excitability, and firing. To achieve these goals, inhibitory synapses themselves undergo several forms of plasticity via diverse mechanisms, strengthening and weakening phasic inhibition in response to numerous activity-induced stimuli. These mechanisms include changing the number and arrangement of functional GABARs within the inhibitory postsynaptic domain (iPSD), which can profoundly regulate inhibitory synapse strength.
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