This paper presents a rigorous and comprehensive nonlinear circuit-theoretic foundation for the memristive Hodgkin-Huxley Axon Circuit model. We show that the Hodgkin-Huxley Axon comprises a potassium ion-channel memristor and a sodium ion-channel memristor, along with some mundane circuit elements. From this new perspective, many hitherto unresolved anomalous phenomena and paradoxes reported in the literature are explained and clarified. The yet unknown nonlinear dynamical mechanisms which give birth to the action potentials remain hidden within the memristors, and the race is on for uncovering the ultimate truth.
Analog hardware architecture of a memristor bridge synapse-based multilayer neural network and its learning scheme is proposed. The use of memristor bridge synapse in the proposed architecture solves one of the major problems, regarding nonvolatile weight storage in analog neural network implementations. To compensate for the spatial nonuniformity and nonideal response of the memristor bridge synapse, a modified chip-in-the-loop learning scheme suitable for the proposed neural network architecture is also proposed. In the proposed method, the initial learning is conducted in software, and the behavior of the software-trained network is learned by the hardware network by learning each of the single-layered neurons of the network independently. The forward calculation of the single-layered neuron learning is implemented on circuit hardware, and followed by a weight updating phase assisted by a host computer. Unlike conventional chip-in-the-loop learning, the need for the readout of synaptic weights for calculating weight updates in each epoch is eliminated by virtue of the memristor bridge synapse and the proposed learning scheme. The hardware architecture along with the successful implementation of proposed learning on a three-bit parity network, and on a car detection network is also presented.
The proper functioning of the endoplasmic reticulum (ER) is crucial for multiple cellular activities and survival. Disturbances in the normal ER functions lead to the accumulation and aggregation of unfolded proteins, which initiates an adaptive response, the unfolded protein response (UPR), in order to regain normal ER functions. Failure to activate the adaptive response initiates the process of programmed cell death or apoptosis. Apoptosis plays an important role in cell elimination, which is essential for embryogenesis, development, and tissue homeostasis. Impaired apoptosis can lead to the development of various pathological conditions, such as neurodegenerative and autoimmune diseases, cancer, or acquired immune deficiency syndrome (AIDS). Calcium (Ca2+) is one of the key regulators of cell survival and it can induce ER stress-mediated apoptosis in response to various conditions. Ca2+ regulates cell death both at the early and late stages of apoptosis. Severe Ca2+ dysregulation can promote cell death through apoptosis. Action potential, an electrical signal transmitted along the neurons and muscle fibers, is important for conveying information to, from, and within the brain. Upon the initiation of the action potential, increased levels of cytosolic Ca2+ (depolarization) lead to the activation of the ER stress response involved in the initiation of apoptosis. In this review, we discuss the involvement of Ca2+ and action potential in ER stress-mediated apoptosis.
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