Introduction to botulinum toxin
Michael Parker, Charlie James in Fundamentals for Cosmetic Practice, 2022
The axon is a long tubular structure which extends out of the cell body. The point of attachment to the cell body is known as the axon hillock, and it is at this point where an action potential is usually generated, a change in the polarisation of a neuron to allow propagation of a signal. The axon is surrounded by a myelin sheath which serves to insulate the axon and decrease the loss of electrical signal, similar to electrical cabling in your home. Neuronal impulses do not travel through the axon but skip along the outside of the myelin sheath between areas known as nodes of Ranvier. At the end of the axon is the axon terminal, a specialised region of finger-like projections which are in close proximity with but not touching another nerve or effector cells (such as muscle). See Figure 8.1. The point at which a neuron interacts with another cell is known as a synapse. A synapse is a gap between axon terminals and the next cell, for example a dendrite of another neuron. A synapse is broken down into the presynaptic terminal of the cell conducting an electrical signal and a postsynaptic terminal, which is the region which receives said signal. There are two main types of synapse: electrical and chemical (Figure 8.2).
Exploring the types and manifestation of disorders
Jane Hanley, Mark Williams in Fathers and Perinatal Mental Health, 2019
The cause of post-traumatic stress disorder is the only major mental disorder that is now understood. One of the major pathophysiological bases for PTSD is caused by multiple molecular pathways causing an excess of excitatory signalling. Synapses are junctions which allow a neuron to electrically or chemically transmit a signal from one cell to another. They can be excitatory or inhibitory. Inhibitory synapses decrease the probability of the firing action of a potential of a cell, whilst the excitatory synapses increase its likelihood, causing a positive action in potential neurons and cells. This excess signalling within the limbic system can lead to intense emotional reactions being triggered by traumatic events. This forces the logical part of the brain to process emotional information, making it more difficult to control thoughts. There is now increasing evidence to suggest that dopamine, responsible for motivation, reward prediction and addiction, is now crucial in the regulation of fear and anxiety (Amorapanth et al. 2000, Yehuda & LeDoux 2007, Glover et al. 2011).
The Chemistry of the Brain
Gail S. Anderson in Biological Influences on Criminal Behavior, 2019
Neurons (or nerve cells) are specialized cells in the nervous system that transmit signals from one part of the body to another and instruct the body on how to act. For a greatly simplified example, imagine nerve cells sending signals through the neural systems to the hand to pick up a fork, use it to pick up a piece of broccoli, and then move the hand up to the mouth to deposit the food therein. Other signals tell the mouth to close the lips, so the food will not fall out, and signals are sent to the mouth to chew, to the glands in the mouth to start secreting digestive enzymes, and so on. This is greatly simplified but gives an idea of the messages going through your body in nanoseconds. There are many other kinds of nerve cells that we do not need to go into here, but it is essential to learn a little more about how nerve cells communicate. The communications take place between junctions called synapses. Figure 9.1 shows two nerve cells communicating. The cell sending the message uses the axon’s synaptic terminals, and the dendrites of the receiving cell receive the message. The transmitting cell is called the presynaptic cell (Figure 9.1), and the cell receiving the signal is called the postsynaptic cell (inset). There are two main types of synapses: (1) electrical synapses, which conduct electrical signals, and (2) chemical synapses, which conduct chemical signals. It is the chemical ones in which we are interested.
The neurosciences at the Max Planck Institute for Biophysical Chemistry in Göttingen
Published in Journal of the History of the Neurosciences, 2023
Heinz Wässle, Sascha Topp
Synapses are the points of contact between individual neurons and mediate the signal transfer in the nervous system. The term synapse was introduced in 1897 by the British neurophysiologist and later Nobel laureate Charles Sherrington (1857–1952), long before its structure and function were clarified (Valenstein 2005, 4) and, above all, against the bitter resistance of the so-called “reticularists,” who believed that nerve cells formed a syncytium (Nissl 1903). In the first half of the last century, first the functional roles of synapses were studied—that is, the chemical signal transmission by a neurotransmitter, its quantal release, and its effect on the postsynaptic nerve cells. When electron microscopy, which had been developed from the 1930s onward, came into use in 1954 (Hentschel 2014, 311; Ruska 1955), it became possible to examine the structure of the synapses, showing that they contained large quantities of small blisters known as vesicles and that the membranes are thickened at the contact points (Figure 3; see De Robertis 1964, 27–48; Cowan and Kandel 2001, 1–87).
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).
C. elegans MAGU-2/Mpp5 homolog regulates epidermal phagocytosis and synapse density
Published in Journal of Neurogenetics, 2020
Salvatore J. Cherra, Alexandr Goncharov, Daniela Boassa, Mark Ellisman, Yishi Jin
Synapses enable the transmission and integration of information within the nervous system. Proper synaptic connectivity is essential to govern nervous system functions such as sensory perception, learning, and coordinated movement. Aberrant synaptic connections have been associated with a variety of neurological disorders. Synapse formation, elimination, and maintenance work together to ensure precision and plasticity of neuronal circuits throughout the lifetime of an animal. Many neuronal-intrinsic mechanisms involve various classes of cell surface proteins and intracellular signaling pathways that establish synaptic connections (Cherra & Jin, 2015; de Wit & Ghosh, 2016; Sudhof, 2018). Additional work has shown how extrinsic mechanisms involving non-neuronal cells, such as astrocytes and microglia, cooperate with neurons to modulate neuronal circuits (Allen & Eroglu, 2017; Chung, Allen, & Eroglu, 2015). It is now well established that astrocytes and microglia play an active role in the pruning of synaptic connections during development of the visual system in mice (Chung et al., 2013; Stevens et al., 2007). In Drosophila, glial cells also remove synapses and axonal components as a means to eliminate neuronal connections (Awasaki et al., 2006; Fuentes-Medel et al., 2009).