• JSTS:Journal of Semiconductor Technology and Science
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• v.14 no.4
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• pp.383-390
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• 2014

This paper presents an excitatory CMOS neuron oscillator circuit design, which can synchronize two neuron-bursting patterns. The excitatory CMOS neuron oscillator is composed of CMOS neurons and CMOS excitatory synapses. And the neurons and synapses are connected into a close loop. The CMOS neuron is based on the Hindmarsh-Rose (HR) neuron model and excitatory synapse is based on the chemical synapse model. In order to fabricate using a 0.18 um CMOS standard process technology with 1.8V compatible transistors, both time and amplitude scaling of HR neuron model is adopted. This full-chip integration minimizes the power consumption and circuit size, which is ideal for motion control unit of the proposed bio-mimetic micro-robot. The experimental results demonstrate that the proposed excitatory CMOS neuron oscillator performs the expected waveforms with scaled time and amplitude. The active silicon area of the fabricated chip is $1.1mm^2$ including I/O pads.

• Journal of Ginseng Research
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• v.47 no.2
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• pp.302-310
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• 2023

Background: The most common type of dementia, Alzheimer's disease (AD), is marked by the formation of extracellular amyloid beta (Aβ) plaques. The impairments of axons and synapses appear in the process of Aβ plaques formation, and this damage could cause neurodegeneration. We previously reported that non-saponin fraction with rich polysaccharide (NFP) from Korean Red Ginseng (KRG) showed neuroprotective effects in AD. However, precise molecular mechanism of the therapeutic effects of NFP from KRG in AD still remains elusive. Methods: To investigate the therapeutic mechanisms of NFP from KRG on AD, we conducted proteomic analysis for frontal cortex from vehicle-treated wild-type, vehicle-treated 5XFAD mice, and NFP-treated 5XFAD mice by using nano-LC-ESI-MS/MS. Metabolic network analysis was additionally performed as the effects of NFP appeared to be associated with metabolism according to the proteome analysis. Results: Starting from 5,470 proteins, 2,636 proteins were selected for hierarchical clustering analysis, and finally 111 proteins were further selected for protein-protein interaction network analysis. A series of these analyses revealed that proteins associated with synapse and mitochondria might be linked to the therapeutic mechanism of NFP. Subsequent metabolic network analysis via genome-scale metabolic models that represent the three mouse groups showed that there were significant changes in metabolic fluxes of mitochondrial carnitine shuttle pathway and mitochondrial beta-oxidation of polyunsaturated fatty acids. Conclusion: Our results suggested that the therapeutic effects of NFP on AD were associated with synaptic- and mitochondrial-related pathways, and they provided targets for further rigorous studies on precise understanding of the molecular mechanism of NFP.