China
Africa
Explore chapters and articles related to this topic
The Neuromuscular Junction
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The neuromuscular junction is a type of chemical synapse in which the depolarization due to an AP in the presynaptic neuron triggers the release of a neurotransmitter from the presynaptic membrane. The neurotransmitter is ACh in the case of the neuromuscular junction.
The Chemistry of the Brain
Published in Gail S. Anderson, Biological Influences on Criminal Behavior, 2019
At a chemical synapse, there is a very narrow gap called a synaptic cleft that separates the transmitting, or presynaptic, cell from the receiving, or postsynaptic, cell. An electrical signal cannot span the gap, but a chemical signal can. So, the electrical signal in the first cell is converted into a chemical messenger (or signal), so it can travel over the cleft. It is then converted back into an electrical signal in the receiving cell, so the receiving cell knows what the message is.
Neurotransmitters and pharmacology
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Ronald A. Browning, Richard W. Clough
The classical neurotransmitters (listed above) are small, water-soluble, organic amines that are synthesized from precursors within the axon terminal and taken into and stored in small round or ovoid vesicles. The synaptic vesicles release their neurotransmitter from the nerve terminal in a voltage- and calcium-dependent process when an “action potential” (AP) or nerve impulse reaches the nerve terminal. Synaptic transmission involves a highly complex and cascading series of molecular events, but the basic steps associated with neurotransmitter release at a chemical synapse are as follows:
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].
MRI biomarkers of disease progression and conversion to secondary-progressive multiple sclerosis
Published in Expert Review of Neurotherapeutics, 2020
Eleonora Tavazzi, Robert Zivadinov, Michael G. Dwyer, Dejan Jakimovski, Tarun Singhal, Bianca Weinstock-Guttman, Niels Bergsland
There is also increasing evidence for widespread synaptic injury in MS [141–143], which can occur independent of gray and white matter demyelination and neuronal loss [142]. This synaptic injury may be accentuated in progressive multiple sclerosis [143] and contribute to the clinically-observed functional decline, despite plateauing of new lesion formation. The neuronal chemical synapse is particularly vulnerable to injury, due to its high bioenergetic requirements [144]. Synaptic vesicle glycoprotein 2 (SV2) is a family of 12-transmembrane domain glycoproteins expressed in the synaptic vesicles in the presynaptic compartment [145]. PET agents targeting SV2a, particularly [C-11]UCB-J, have been recently developed for in vivo assessment of synaptic density in humans [145]. Assessment of synaptic density using [C-11]UCB-J and other novel SV2a PET ligands is an emerging area in MS research.
In vitro models of neuromuscular junctions and their potential for novel drug discovery and development
Published in Expert Opinion on Drug Discovery, 2020
Olaia F Vila, Yihuai Qu, Gordana Vunjak-Novakovic
The neuromuscular junction (NMJ) is the chemical synapse between a motoneuron and a skeletal muscle fiber that enables muscle contraction and allows for voluntary motor movement. NMJ formation is controlled by interactions between motoneurons, skeletal muscle fibers, and glial cells [1]. In vertebrates, the presynaptic motor nerve terminal dictates the synthesis, storage, and release of the neurotransmitter acetylcholine (ACh) and agrin [2]. When an action potential reaches the presynaptic terminal and activates voltage-gated calcium channels, calcium enters the neuron and triggers the diffusion of ACh across the synaptic cleft to the acetylcholine receptors (AChRs) on the postsynaptic muscle membrane. Activation of these receptors leads to opening of cation channels in the muscle membrane, producing its depolarization. Meanwhile, acetylcholinesterases located within the synaptic cleft degrade the acetylcholine, allowing the NMJ to return to its resting state.