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Neuronal Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Synaptic transmission in mammals usually occurs via chemical neurotransmitters (Figure 4.12). The presynaptic terminal is depolarized by an action potential, which opens voltage-gated calcium channels; calcium ions flow into the presynaptic terminal and cause neurotransmitter vesicles to fuse with the presynaptic membrane. The neurotransmitter is thus released into the synaptic cleft by exocytosis; it diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane and alters its permeability. The receptors in the postsynaptic membrane may be either ion channels or coupled with G proteins, which activate a second messenger system.
Computational Neuroscience and Compartmental Modeling
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
Usually, we can treat an axon as a simple delay line for the propagation of action potentials, although it could also be, modeled as a series of compartments if we were interested in understanding the details of axonal propagation. In most cases, the change in the postsynaptic channel conductance is a simple function of time, which may be determined from experimental measurements. Then, we may avoid having to model the details of the process of presynaptic transmitter release, and it’s binding to postsynaptic receptors, and the way in which the permeability of the postsynaptic membrane is affected. Instead, we may use an analytical expression such as the alpha function, described in Chapter 6, to represent the resulting conductance of synaptically activated channels. When more detailed models of the biochemical reactions underlying synaptic transmission are required, they may be created using the techniques described in Chapter 10 and the graphical interface Kinetikit, which was created for the development of models of biochemical signaling pathways.
Histology and Pathology of the Human Neuromuscular Junction with a Description of the Clinical Features of the Myasthenic Syndromes
Published in Marc H. De Baets, Hans J.G.H. Oosterhuis, Myasthenia Gravis, 2019
F.G.I. Jennekens, H. Veldman, John Wokke
Immunohistochemistry of AChRs demonstrates that staining of the postsynaptic membrane is weak at some places, indicating decreased density of the receptors123 (Figure 14). Deficiency of AChRs on muscle fibers has been confirmed by measurement of125 I-alpha-BTX binding.124,125 Staining of AChRs is sometimes seen on degraded membrane products in the synaptic basal lamina. Loss of receptors can apparently also be caused by extracellular breakdown of postsynaptic membrane. Not all postsynaptic membranes are however affected to the same degree. The antibodies also bind to extrajunctional (fetal) receptors; potentially this may lead to structural changes of myofibers in the early fetal period.
Efficient simulations of stretch growth axon based on improved HH model
Published in Neurological Research, 2023
Xiao Li, Xianxin Dong, Xikai Tu, Hailong Huang
Neuronal cell is composed of three components: a cell body, an axon, and a dendrite. These components are responsible for receiving, integrating, and delivering information. In general, neurons receive and integrate information from other neurons via their dendrites and cell bodies, and then transfer it to other neurons via their axons. Nerve fibers have great excitability and conductivity, and their primary role is to transmit information between neurons. When a sufficient stimulus excites a nerve fiber, it immediately generates a propagable action potential. Chemical synapses allow action potentials to be passed from one neuron to the next by transporting neurotransmitters through synaptic vesicles. The action potential-induced shift in membrane potential causes the calcium channel on the synaptic terminal membrane to open, allowing a substantial number of calcium ions to flow into the membrane, resulting in an abrupt increase in calcium ions in the synaptic membrane. When synaptic vesicles detect an increase in the number of calcium ions in the surrounding environment, they fuse with the presynaptic membrane and spit neurotransmitters into the synaptic gap. After binding to a protein receptor on the postsynaptic membrane, the neurotransmitter causes excitement or inhibition.
Regulation of LTP at rat hippocampal Schaffer-CA1 in vitro by musical rhythmic magnetic fields generated by red-pink (soothing) music tracks
Published in International Journal of Radiation Biology, 2023
Zijia Jin, Lei Dong, Lei Tian, Mei Zhou, Yu Zheng
It is well known that when presynaptic afferent fibers are stimulated, the neurotransmitter glutamate is released into the synaptic gap, Na+, and K+ ion channels open the triggering postsynaptic membrane depolarization, removal of Mg2+ from NMDA receptor channels, and a large Ca2+ inward flow, leading to an increase in postsynaptic Ca2+ concentration and protein kinase activation, which triggers an increase in the number and conductivity of AMPA receptors on the postsynaptic membrane, and LTP is induced (Abbas et al. 2015). As a physical intervention, time-varying magnetic field has its effect on ions, receptors and other intermediate factors. Tokay et al. found that NMDA receptors are activated by high intensity 100 Hz magnetic field and directly induce LTP production (Tokay et al. 2014). Magnetic field stimulation at different frequencies may exert excitatory or inhibitory effects on cells by altering the ion distribution inside and outside the cell membrane or the permeability of channel proteins on the cell membrane (Hossmann and Hermann 2003), which may influence neuronal function. Maskey et al. found experimentally that magnetic field radiation at low frequencies may have an inhibitory effect on the function of cells. (Maskey et al. 2010) and even caused severe cellular damage if exposed to magnetic fields for a long time (Bas et al. 2009). The magnetic field stimulation with a frequency larger than 1500 Hz may have a different mechanism of action when acting on cells compared with that lower than 1500 Hz, resulting in different effects of the two.
Lack of bombesin receptor-activated protein homologous protein impairs hippocampal synaptic plasticity and promotes chronic unpredictable mild stress induced behavioral changes in mice
Published in Stress, 2023
Xueping Yao, Xiaoqun Qin, Hui Wang, Jiaoyun Zheng, Zhi Peng, Jie Wang, Horst Christian Weber, Rujiao Liu, Wenrui Zhang, Ji Zeng, Suhui Zuo, Hui Chen, Yang Xiang, Chi Liu, Huijun Liu, Lang Pan, Xiangping Qu
PSD95 is one of the major regulators of synaptic maturation and acts as an essential scaffolding protein during synaptogenesis. It was reported to interact, stabilize and help N-methyl-D-aspartic acid receptors (NMDARs) traffic to the postsynaptic membrane and is required for synaptic plasticity associated with NMDA receptor signaling (Chen et al., 2011). No significant loss of PSD95 was observed in hippocampal sections from bc004004−/−mice compared with wild type control mice (Figure 6(A,C)). Western blot analysis of PSD95 in the hippocampal tissues is shown in Figure 6(E,G). Although the main effect of genotype (F (1, 5) = 10.54, p = .02) was significant, further pairwise comparison did not find significant difference on PSD95 expression between knockout mice and control mice. The main effect of CUMS treatment (F (1, 5) = 6.55, p = .05) was not significant and there was no interaction between CUMS treatment and genotype (F (1, 5) = 0.39, p = .56).