Bio-mimetic advanced electronic systems are emerging rapidly, engrossing their applications in neuromorphic computing, humanoid robotics, tactile sensors, and so forth. The biological synaptic and nociceptive functions are governed by intricate neurotransmitter dynamics that involve both short-term and long-term plasticity. To emulate the neuronal dynamics in an electronic device, an Ag/TiO/Pt/SiO/Si memristor is fabricated, exhibiting compliance current controlled reversible transition of volatile switching (VS) and non-volatile switching (NVS). The origin of the VS and NVS depends on the diameter of the conducting filament, which is explained using a field-induced nucleation theory and validated by temporal current response measurements. The switching delay of the device is used to determine the characteristic nociceptive behaviors such as threshold, relaxation, inadaptation, allodynia, and hyperalgesia. The short-term and long-term retention loss attributed to the VS and NVS, respectively, is used to emulate short-term memory and long-term memory of the biological brain in a single device. More importantly, synergistically modulating the VS-NVS transition, the complex spike rate-dependent (SRDP) and spike time-dependent plasticity (STDP) with a weight change of up to 600% is demonstrated in the same device, which is the highest reported so far for TiO memristors. Furthermore, the device exhibits very low power consumption, ∼3.76 pJ/spike, and can imitate synaptic and nociceptive functions. The consolidation of complex nociceptive and synaptic behavior in a single memristor facilitates low-power integration of scalable intelligent sensors and neuromorphic devices.
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http://dx.doi.org/10.1021/acsami.3c02727 | DOI Listing |
Acid-sensing ion channels (ASICs) are typically activated by acidic environments and contribute to nociception and synaptic plasticity. ASIC1a is the most abundant subunit in the central nervous system and forms homomeric channels permeable to Na and Ca , making it a compelling therapeutic target for acidotic pathologies including stroke and traumatic brain injury. However, a complete conformational library of human ASIC1a in its various functional states has yet to be described.
View Article and Find Full Text PDFSci Adv
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Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4970, USA.
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Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
J Pharmacol Sci
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Laboratory of Pharmacology, School of Pharmaceutical Sciences, Kitasato University, 5-9-1, Shirokane, Minato-ku, Tokyo, 108-8641, Japan; Medicinal Research Laboratories, School of Pharmacy, Kitasato University, 5-9-1, Shirokane, Minato-ku, Tokyo, 108-8641, Japan. Electronic address:
Brain Sci
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Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Neuropathic pain is challenging to treat, often resistant to current therapies, and associated with significant side effects. Pregabalin, an anticonvulsant that modulates calcium channels, is effective but can impair mental and motor functions, especially in older patients. To improve patient outcomes, reducing the doses of pregabalin and combining it with other drugs targeting different neuropathic pain mechanisms may be beneficial.
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