ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
A neuron consists of the SOMA or cell body, dendrites (see DENDRITE) and the AXON. The soma is the site of the synthesis of PROTEINS, and contains the NUCLEUS and various subcellular organelles including MITOCHONDRIA, RIBOSOMES, ENDOPLASMIC RETICULUM, GOLGI APPARATUS and LYSOSOMES. The term PERIKARYA is often used interchangeably with the soma, but strictly speaking, it refers to the CYTOPLASM around the nucleus. From the soma emerge a number of dendrites, usually two to five, which branch into secondary and higher-order dendrites. The function of dendrites is to receive synaptic inputs. The axon emerges from either the soma or a main dendrite. Although a neuron usually has a single axon, axons may branch to innervate multiple targets. The function of the axon is to conduct action potentials, and release neurotransmitters at axon terminals. Axons can be myelinated (see MYELIN) or unmyelinated. Myelinated axons have the NODES OF RANVIER, which are gaps in myelin that allow faster conduction of action potentials. The action potential is generated at the AXON HILLOCK, the cone-shaped site where the axon originates.
The movement systems: skeletal and muscular
Nick Draper, Helen Marshall in Exercise Physiology, 2014
The identification of the two main muscle fibre types originates from early research into the structure and function of muscles. In the 19th Century researchers identified differences in muscle fibre types that were visible to the naked eye. In 1873 Louis Ranvier (1835–1922), who in other research identified the presence of a myelin sheath around nerve fibres (the gaps in the sheath, the nodes of Ranvier, being named after him), published a paper detailing structural differences in the white and red muscle tissue of rabbits and rays. This difference can be seen in chickens where the legs, which appear red in colour, comprise a higher proportion of type I fibres, whereas the breast and wings, which appear white, contain more type II fibres. The difference in colour between the two fibre types is due to the presence of a higher concentration of myoglobin (oxygen-binding protein) and increased capillarity within type I fibres.
Local Anesthetics and Additives
Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand in Pediatric Regional Anesthesia, 2019
This all-or-none mechanism of conduction at the surface of the axonal membrane is operative in unmyelinated (C) fibers, whereas it is markedly modified by the presence of myelin, which plays the role of an insulating sheath. At the nodes of Ranvier, the axonal membrane is enriched in sodium channels and thus is markedly more excitable than the rest of the cell membrane. Since it also directly contacts the extracellular fluid at this level, depolarizing impulses can “jump” from node to node. This saltatory conduction considerably speeds the transmission of impulses in myelinated fibers. Since the (regular) intervals between adjacent nodes of Ranvier increase with the thickness of both the nerve fiber and the myelin sheath, the conduction speed increases with the size of the nerve fibers, from unmyelinated C fibers to large myelinated Aα fibers Figure 3.5 and Table 3.4).
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
The compressive forces that accompany spinal cord insults are also responsible for oligodendrocyte necrosis and necroptosis within days of the injury, eventually contributing to myelin damage [10,11]. As the injury progresses, accumulation of cytotoxic factors in the microenvironment causes oligodendrocytes to undergo apoptosis in a similar manner to neurons. This ultimately eradicates the associated myelin sheath [11,12]. ROS in the microenvironment can react with the lipids in the cell membrane of myelinating oligodendrocytes and results in the oxidative degradation and peroxidation of lipids (reviewed by Plemel et al. [12]). The products of lipid peroxidation interact with membrane receptors and transcription factors/repressors to induce signaling for apoptosis. This can stimulate the activation of both the intrinsic and extrinsic apoptotic signaling pathways [13]. Moreover, disorganization of the nodes of Ranvier occurs through the diffusion of nodal, paranodal and juxtaparanodal ion channels within hours of the injury, and is found to persist at 6 weeks following injury, ultimately disrupting signal transduction [14,15]. The denuded axons that have lost their metabolic and protective support from the associated myelin sheath are also vulnerable to Wallerian degeneration, which degenerates the neurons that had otherwise been spared during the initial traumatic mechanical insult [16].
Burst and high frequency stimulation: underlying mechanism of action
Published in Expert Review of Medical Devices, 2018
Shaheen Ahmed, Thomas Yearwood, Dirk De Ridder, Sven Vanneste
HF SCS has the ability to generate rapid and reversible conduction block – a block of neural activity – by inactivating sodium channels along several nodes of Ranvier, as demonstrated in a peripheral nerve model and confirmed by animal models [41,42]. Indeed, it has been proposed that HF SCS blocks paresthesia by stopping large-diameter fibers from generating action potentials (fibers greater than 15–18 µm begin to shut down at 4 kHz and 8–9 µm fibers begin to shut down at 8 kHz) and, instead, activating medium- and small-diameter fibers that reduce WDR cell signaling encoding neuropathic pain [43]. However, recent computer simulation models show that conduction block thresholds are almost always outside of the clinical amplitude range. This fits with other research that states that, before a conduction block is generated with HF SCS, there is an initial increase in action potential firing called the onset response. This onset response can be observed by recording increased activity in WDR and manifests behaviorally as a feeling of discomfort during the first few minutes of stimulation [44]. Although this onset response has been observed in animal models of HF SCS, no paresthesia or other subjective perceptions have been reported during clinically effective HF SCS in human patients [22]. These findings suggest that HF SCS may not function explicitly through direct activation or conduction block of spinal cord fibers, but rather through more complex and subtle mechanisms for pain relief.
Temperature sensitivity in multiple sclerosis: An overview of its impact on sensory and cognitive symptoms
Published in Temperature, 2018
Aikaterini Christogianni, Richard Bibb, Scott L Davis, Ollie Jay, Michael Barnett, Nikos Evangelou, Davide Filingeri
Mechanistically, it would appear that demyelination reduces the axon safety factors, such that less current is available to excite nodes of Ranvier and to propagate action potentials effectively along the axon (Figure 1) [1]. Furthermore, there is evidence that segmental axonal demyelination in MS unmasks an increased density of membrane potassium channels with a high predilection for current leak via potassium efflux with new sodium channels also being inserted within the axonal membrane as an ion channel adaptation to demyelination [101]. Interestingly, the newly incorporated sodium channels exhibit an altered high sensitivity to temperature-induced pore closure, where elevations in temperature of as little as 0.2–0.5°C are sufficient to compromise action potential depolarization [101]. The picture that emerges is that a combination of changes in the intrinsic excitability of demyelinated fibers and in the temperature sensitivity of the ion channels that contribute to their resting membrane potentials, result in the conduction slowing and/or block that is typical of Uhthoff’s phenomena.
Related Knowledge Centers
- Action Potential
- Anatomy
- Axolemma
- Axon
- Extracellular Space
- Saltatory Conduction
- Myelin
- Neuroscience
- Ion Channel
- Ion