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Technological Evolution of Wireless Neurochemical Sensing with Fast-Scan Cyclic Voltammetry
Published in Iniewski Krzysztof, Integrated Microsystems, 2017
Dan P. Covey, Kevin E. Bennet, Charles D. Blaha, Pedram Mohseni, Kendall H. Lee, Paul A. Garris
Neurons communicate via bioelectric and chemical signals [1]. As illustrated in Figure 7.1, communication along the length of one neuron’s axon is achieved by conduction of the axon potential, a relatively large bioelectric signal originating from a transient (millisecond) change in membrane potential mediated by the flux of ions, typically Na+ and K+, through protein channels. The influx of Ca2+ at the axon terminal elicits the release of neurotransmitters from their vesicular package into the extracellular gap between two neurons separated by the synaptic cleft. These chemical messengers are released from the presynaptic neuron in response to the action potential, diffuse across the cleft, and bind to specific protein receptors on the postsynaptic neuron, where the chemical signal is transduced back into a bioelectric signal. Released neurotransmitters are typically taken up again into the presynaptic neuron to terminate synaptic signaling. Fast conduction velocities of the action potential (upwards of several meters per second) and the minimal delay for the neurotransmitter to diffuse across the short, ~25-nm distance of the cleft (milliseconds or less) ensure rapid, long- distance neuronal communication.
In vitro studies
Published in Ze Zhang, Mahmoud Rouabhia, Simon E. Moulton, Conductive Polymers, 2018
A. Lee Miller, Huan Wang, Michael J. Yaszemski, Lichun Lu
The axon leaves the neuronal cell body at an enlarged region called the axon hillock (Fuortes et al. 1957). It travels away from the soma for a greater distance before it becomes axon terminals, tiny branches that form synapses with other cells. An action potential propagates along the axon, reaches axon terminals, and induces a localized rise in the level of Ca2+, causing vesicles in the axon terminal to release neurotransmitters into the synaptic cleft. Dendrites receive chemical signals from the axon termini of other neurons. They convert these signals into small electric impulses and transmit them inward toward the cell body.
The Emergence of Order in Space
Published in Pier Luigi Gentili, Untangling Complex Systems, 2018
When the action potential reaches the synapsis, voltage-gated Ca+2 channels open and calcium ions enter the axon terminals. Ca+2 entry causes neurotransmitter-containing synaptic vesicles to move to the plasma membrane, fuse with it and release their content according to the process of exocytosis. The neurotransmitter diffuses and binds to ligand-gated ion channels of the dendrites of other neurons, exerting either an inhibitory or an excitatory action.
A bulk-driven, buffer-biased, gain-boosted amplifier for biomedical signal enhancement
Published in Cogent Engineering, 2019
Sarin Vijay Mythry, D. Jackuline Moni
When neurons depolarize, Na+ (sodium) channels rapidly open and shift the membrane potential towards the equilibrium potential of sodium. As leakage channels are open at rest, there is a balance between leakage currents and Na+ channels opened at depolarization, but at a specific point, Na+ current exceeds the leakage current, membrane potential at this state is called the threshold potential. However, as Na+ depolarization opens voltage gated K+ channels; the membrane potential overshoots 0 mV and then rapidly returns to resting membrane potential after a transient undershoot. This rapid change occurs over several milliseconds and is called as an Action potential (or commonly as Sodium spike) and this propagates along the length of the axon. At the axon terminal, the spike provides Ca2+ opening depolarization and the resultant release of neurotransmitters which excite another neuron and thereby communicating information (Sadock et al., 0000). Figure 4 depicts the depolarization and repolarization wave in a nerve cell (Sadock et al., 0000).
Carob extract attenuates brain and lung injury in rats exposed to waterpipe smoke
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Mona Abdel-Rahman, Amira A. Bauomy, Fatma Elzahraa H. Salem, Mona Ahmed Khalifa
Wyss et al. [27] reported that amiodarone pass into the brain and it has an anticonvulsant and hypnotic effects. Moreover, amiodarone prolonged the sleeping time and behaved as central nervous system depressant drug in pentobarbital-induced sleeping in rat model [28]. Many reports attributed the anticonvulsant activity of amiodarone to its activity as a multiple ion-channel blocker drug which inhibit Na+, Ca2+ inward and K+ outward currents [28,29] . It well known that when action potentials depolarize the plasma membrane of the axon terminal, voltage-gated Ca2+ channels is open. This permits Ca2+ to diffuse down its concentration gradient into the cytoplasm, where it stimulates the release of neurotransmitters which stored in synaptic vesicles by exocytosis [30]. Because of the amiodarone is a calcium ion-channel blocker [29]; so the neurotransmitters release is inhibited and as the result their content is increased in brain which may explain the increment in neurotransmitters content in some time intervals in the present study.
Mechanism of peripheral nerve modulation and recent applications
Published in International Journal of Optomechatronics, 2021
Heejae Shin, Minseok Kang, Sanghoon Lee
The main structure of the PNS is a nerve that has an enclosed structure like a cable bundle in which neurons are gathered, playing the role of the passage for the electrochemical signals. As shown in Figure 1(a), a neuron consists of a cell body with the nucleus, a dendrite that receives nerve signals, generating an action potential when the signals exceed the threshold, and an axon that transmits the generated signals to an axon terminal to transfer the signal to another neuron. In some cases, this axon is covered with a myelin sheath, making the speed transmission is significantly faster compared to the unmyelinated neurons, which are covered with connective tissue called the endoneurium. In addition, the axon terminal forms a synapse with adjacent neurons, in which the electrical signal transmitted through the axon is converted into a chemical signal by releasing a molecule called a neurotransmitter that is a chemical messenger inhibiting or activating the neuron by influencing the receptor on the targeted neuron or organ. The aggregate of these nerve fibers is called a fascicle, and this fascicle is surrounded by connective tissue called the perineurium. Inside the fascicle, afferent fibers that send afferent (sensory) signals to the CNS and efferent fibers that send efferent (motor) signals from the CNS could be both located in a fascicle or a nerve which is called a mixed nerve fiber. The group of fascicles is called a nerve. A nerve is surrounded by epineurium, and it also consists of blood vessels that provide nutrients for the whole structure. (Figure 1(b)).[10]