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The Neuromuscular Junction
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The synaptic bouton becomes embedded in a small, shallow depression in the muscle, where it is closely apposed to the muscle membrane but separated from it by a synaptic cleft (Figure 5.2). The muscle membrane in the synaptic region is termed the endplate, or the motor endplate. The synaptic bouton contains an abundance of mitochondria and synaptic vesicles of 40–50 nm diameter that are filled with the neurotransmitter acetylcholine (ACh). The endplate is folded into many troughs about 500 nm deep and about 100 nm wide separated by crests of about the same width. The width of the synaptic cleft at the crests of the endplate is about 20–60 nm. Facing the opening of the troughs are thickened regions of the synaptic bouton referred to as active zones. These zones have a high concentration of vesicles, with many of these vesicles touching the inner side of the membrane of the synaptic bouton.
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.
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
The primary synaptic cleft is the space between the presynaptic membrane and an imaginary line that connects the crests of the junctional folds. The spaces between the junctional folds are designated as secondary clefts. The width of the primary cleft is approximately 60 nm and tends to decrease with age (in mice).26 The synaptic basal lamina continues on the one hand in the extrasynaptic basal lamina and on the other hand in the basal lamina of the secondary clefts. Small processes of Schwann cells may intrude at some places into the primary cleft and cover part of the presynaptic membrane. The synaptic basal lamina is sometimes seen to be split into two layers, one covering the presynaptic membrane and the other the postsynaptic membrane.
Combination of tea polyphenols and proanthocyanidins prevents menopause-related memory decline in rats via increased hippocampal synaptic plasticity by inhibiting p38 MAPK and TNF-α pathway
Published in Nutritional Neuroscience, 2022
Qian Yang, Yusen Zhang, Luping Zhang, Xuemin Li, Ruirui Dong, Chenmeng Song, Le Cheng, Mengqian Shi, Haifeng Zhao
Dendritic spines are the major sites of excitatory synaptic input, the number of synapses is closely related to the transmission efficiency and the transmission efficiency of nerve impulses [40]. In the model group, decreased density of dendritic spines and decreased number of excitatory synapses impaired the efficiency of nerve conduction. Therefore, we further observed the ultrastructure of synapses by transmission electron microscope. Structural plasticity of synapses is the basis of functional plasticity, mainly manifested as the size of presynaptic and postsynaptic contact area, the number of active areas in the synaptic contact area, the change of synaptic gap (affecting synaptic transmission efficiency) [41]. Classical parameters of synaptic structure include synapse interface curvature, synapse gap width, postsynaptic density (PSD) thickness and numerical density per unit volume (Nv) [42]. Narrow synaptic cleft is advantageous to the pre-synaptic membrane release of neurotransmitters, larger interface curvature can reduce the neurotransmitters into the surrounding interstitial diffusion ensure the neurotransmitter release further to reach the target, improve the transfer function.
Pharmacologic agents directed at the treatment of pain associated with maladaptive neuronal plasticity
Published in Expert Opinion on Pharmacotherapy, 2022
Joseph V. Pergolizzi, Giustino Varrassi, Peter Magnusson, Frank Breve, Robert B. Raffa, Paul J. Christo, Maninder Chopra, Antonella Paladini, Jo Ann LeQuang, Kailyn Mitchell, Flaminia Coluzzi
A synapse forms when the pre-synaptic terminal of one neuron starts to acquire vesicles at the same time that the post-synaptic portion recruits receptors for neurotransmitters. The synaptic cleft, the gap between pre- and post-synaptic membranes, is the focal point for chemical synapse [8]. An action potential that reaches the presynaptic axon terminal causes membrane depolarization and, in so doing, opens sodium channels of the terminal which allows an influx of positive sodium ions, resulting in the opening of voltage-gated calcium channels and the influx of calcium ions. The calcium ions interact with calcium-sensing proteins at the terminal, enabling them to interact with the soluble N-ethylmaleimide-sensitive factor activating protein receptor proteins [8]. Specialized cell-adhesion molecules can aid in synaptic cell adhesion and stabilize synapses. In that way, it is possible for one neuron to have thousands of synaptic inputs, which help define signaling pathways and synaptic connections [9].
Immune to addiction: how immunotherapies can be used to combat methamphetamine addiction
Published in Expert Review of Vaccines, 2021
Md Kamal Hossain, Majid Hassanzadeganroudsari, Erica Kypreos, Jack Feehan, Vasso Apostolopoulos
In the setting of the natural reward mechanism, dopamine is secreted from presynaptic neuron into the synaptic cleft (Figure 2). The released dopamine stays in the synaptic cleft for a short duration and transmits a signal by propagating an action potential to the postsynaptic neuron. The dopamine is then returned to the presynaptic neuron by a specific dopamine transporter. With application of METH, dopamine remains in the synaptic cleft for 8 to 12 hours, causing ongoing stimulation of the postsynaptic neuron, and extended feelings of euphoria. The critical action of METH on this mechanism is to block the action of the dopamine transporter, leading to the inability to remove the neurotransmitter and subsequent increased concentration in the synaptic cleft. With this large amount of dopamine, and its sustained action on the reward center, the individual experiences an extreme peak of euphoria, leading to addiction [20,24].