Neurological issues
Andrea Utley in Motor Control, Learning and Development, 2018
Action potentials are the means by which the brain receives, analyzes and conveys information, which is determined by the pathway the signal travels to the brain. The transmission of the action potential is speeded up by a lipid membrane surrounding the axon called the myelin sheath (or principally Schwann cells in the PNS). The axon eventually divides into branches, at the end of which are presynaptic terminals; these allow communication with other neurons through the transmission of the electrical impulses. The passage of information from one neuron to another occurs via synapses, where the axon of one neuron comes into close proximity to, but does not touch or communicate anatomically with, another (postsynaptic) nerve cell. The space that separates two neurons is called the synaptic cleft. The electrical activity in the presynaptic neuron is transmitted across the synaptic cleft to the postsynaptic neuron through further electrical activity or a chemical mediator – a neurotransmitter.
Sympathetic Neurotransmission
Kenneth J. Broadley in Autonomic Pharmacology, 2017
The junction between the varicosity and effector cell is the synaptic cleft which varies in distance in different tissues. In the vas deferens, a single axon supplies each muscle fibre (multi-unit) and is deeply embedded in the muscle cell. The Schwann cell covering of the axon becomes incomplete in the varicose region, the naked varicosities making close neuroeffector contact with the smooth muscle cells. The synaptic cleft is only 10–20 nm, known as close junctions. Some muscle cells receive no direct innervation. In contrast, the synaptic cleft of blood vessel smooth muscle is larger at 200 nm or ≥4 μm (Bevan & Su 1973). Terminal sympathetic axons are confined to the adventitio-medial junction and ramify over the smooth muscle surface, rarely penetrating more than two to three cells into the smooth muscle. The released noradrenaline therefore has to penetrate into the muscle layers slowly. Excitation of the inner layers of smooth muscle probably therefore occurs by propagation of the impulse from cell to cell rather than by diffusion of noradrenaline. More recent studies suggest that varicosities do form closer contact (<100nm) in certain arterioles (Luff & McLachlan 1989). The synaptic cleft distance is affected by the contractile activity of innervated tissues.
The Neuromuscular Junction
Nassir H. Sabah in 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.
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].
The role of synaptic biomarkers in the spectrum of neurodegenerative diseases
Published in Expert Review of Proteomics, 2020
Sonia Mazzucchi, Giovanni Palermo, Nicole Campese, Alessandro Galgani, Alessandra Della Vecchia, Andrea Vergallo, Gabriele Siciliano, Roberto Ceravolo, Harald Hampel, Filippo Baldacci
Synapses are the essential component of neural networks and allow transfer and storage of information [3]. The information is transferred from pre-synaptic to post-synaptic neurons by the release of neurotransmitters within the synaptic cleft. Proteins belonging to the so-called SNARE complex tune this vesicle trafficking [4]; these include the synaptosomal-associated protein 25 (SNAP-25), a key adhesion molecule for vesicle docking, trafficking, and exocytosis, whose activity is modulated by synaptotagmin 1 (SYT-1), a pre-synaptic calcium sensor (Figure 1). Neurotransmitters released in the synaptic cleft bind post-synaptic receptors, thus activating downstream intracellular signal pathways. Several post-synaptic proteins further modulate these signals, including Neurogranin (Ng), a protein largely expressed in the dendritic spines of excitatory neurons of the cerebral cortex and of hippocampus [5,6]. Ng is a key modulator of Long-Term Potentiation (LTP), a mechanism largely depending on calcium signaling [7,8] (Figure 1).
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.
Related Knowledge Centers
- Central Nervous System
- Nervous System
- Neuromuscular Junction
- Perception
- Neurotransmitter
- Neuron
- Gland
- Neural Circuit
- Biological Computation
- Thought