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Introduction to botulinum toxin
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
Botulinum toxin is a proteolytic enzyme which functions by inhibiting the secretion of acetylcholine from afferent neurons at the neuromuscular junction. The toxin binds to the cell membrane of neurons which then form a vesicle around it to absorb it across the cell membrane through a process known as endocytosis. As the vesicle is taken through the cell membrane, the contents acidify, causing the vesicle to migrate further within the cell. Once the toxin is within the cytoplasm of an acetylcholine-secreting neurons, it cleaves soluble NSF attachment protein receptors, otherwise known as SNARE proteins. These proteins are essential in the exocytosis of vesicles and their contents from the presynaptic membrane into the presynaptic cleft. By irreversibly inhibiting the exocytosis of acetylcholine, botulinum toxin prevents neurons in the affected area from initiating movement at motor muscle endplates. In the realm of cosmetics, this prevents muscular movement and wrinkle formation.
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
Active zones are densely coated parts of the presynaptic membrane. They are lined by large intramembranous particles considered to be the voltage gated presynaptic calcium channels.24 The dense material of the active zones contains cytoskeletal proteins required for docking of synaptic vesicles. Depolarization of the presynaptic membrane causes opening of the calcium channels and influx of Ca2+ ions. The influx triggers fusion of docked synaptic vesicles with the plasma membrane and exocytosis of vesicle content. Ca2+ becomes stored in mitochondria and probably in synaptic vesicles (see Chapter 3). The proteins of the synaptic membrane form pits in the presynaptic membrane and become covered with clathrin. These membranes are reclaimed and recognizable as coated vesicles that are removed from the active zones. The coat is lost and the vesicles become reloaded with ACh. Processes involved in synaptic vesicle membrane endocytosis are closely related to those of receptor-mediated endocytosis (see for review reference 25).
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.
The neurosciences at the Max Planck Institute for Biophysical Chemistry in Göttingen
Published in Journal of the History of the Neurosciences, 2023
Whittaker and his colleagues were able to show that the neurotransmitters were not released from the cytoplasmic pool, but through fusion of the vesicle with the presynaptic membrane. They were also able to demonstrate that vesicles are “created” in the cell body and are then transported to the synapse in Fast Axonal Transport. Following vesicle fusion with the presynaptic membrane when the neurotransmitters are released, there is a reuptake of the vesicle, which is once again loaded with neurotransmitters. Whittaker and his colleagues studied this vesicle cycle with radioactive marker substances (e.g., Dextran) and with antibodies against specific proteoglycanes they had identified in the vesicle membranes. They also identified and localized other elements of the vesicle membrane. Figure 4 shows how far their knowledge had reached in the year 1984 (Whittaker 1984).
Morphology changes in the cochlea of impulse noise-induced hidden hearing loss
Published in Acta Oto-Laryngologica, 2022
Guowei Qi, Lei Shi, Handai Qin, Qingqing Jiang, Weiwei Guo, Ning Yu, Dongyi Han, Shiming Yang
The synapse between inner hair cell and type I spiral ganglion neuron is called ribbon synapse, which is characterized by the presynaptic ribbon-like structure. This research mainly focused on the low spontaneous rate (Low-SR) ribbon synapse, which is located in the modiolar side of the inner hair cell and is more vulnerable to noise. In normal group, the typical ribbon synapse contains a rugby-ball-like ribbon structure, around which anchored synapse vesicles contain glutamate (Figure 4(a)). One month after impulse noise exposure, part of the Low-SR ribbon synapses in the NIHHL group were impaired (Figure 4(f)). The typical ribbon structure was replaced by a bulk of irregular-shaped electron-dense substance on the presynaptic membrane, with synapse vesicles anchored loosely around it. At the same time, some ribbon synapses remained intact (Figure 4(b, e)). Compared with the normal group, no difference was found in the post-synapse structure. In the NIHL group, the ribbon synapse was more seriously damaged. Though typical post synapse structure can be found in the modiolar side of the inner hair cell, no ribbon structure was found through transmission electron microscopy observation of consecutive sections in adjacent areas, which means high-intensive impulse noise exposure can destroy the presynaptic ribbon structure (Figure 4(c, g)).