Academic literature on the topic 'Myelinated / Unmyelinated axon'
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Journal articles on the topic "Myelinated / Unmyelinated axon"
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Jaffe, Richard A., and Michael A. Rowe. "Differential Nerve Block." Anesthesiology 84, no. 6 (June 1, 1996): 1455–64. http://dx.doi.org/10.1097/00000542-199606000-00022.
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Background Clinically, differential block is manifested by the loss of small fiber mediated sensation (e.g., temperature) two or more dermatomes beyond the sensory limit for large fiber mediated sensations. These observations support the belief that sensitivity to local anesthetics is inversely proportional to axon diameter. This study reports the first measurements of differential sensitivity to lidocaine in individual myelinated and unmyelinated mammalian dorsal root axons. Methods Lumbar dorsal roots and vagus nerves were isolated from anesthetized adult rats and maintained in vitro in a perfusion/recording chamber at 37 +/- 0.3 degrees C. Using single fiber techniques, evoked action potentials in individual myelinated and unmyelinated axons were digitized and recorded for subsequent analysis. Axons were exposed to lidocaine at 150, 260, or 520 microM. Sensitivity to local anesthetic was assessed by measuring the incidence of conduction block and the magnitude of conduction velocity slowing under steady-state conditions. Results Data were obtained from 77 dorsal root axons and 41 vagal axons. The estimated steady-state EC50 lidocaine concentration for myelinated dorsal root axons (232 microM) was comparable to that for unmyelinated axons (228 microM). Similarly, the incidence of conduction block was not significantly different among dorsal root axon groups. However, unmyelinated dorsal root axons were significantly less sensitive to the conduction velocity slowing effect of lidocaine than their myelinated counterparts (P < 0.01). The incidence of conduction block in short (mean length 13.5 mm) dorsal root axons was not significantly different from that in long (mean length 22.4 mm) axons. Compared with dorsal root axons, the estimated EC50s for vagal myelinated and unmyelinated axons (345 and 285 microM, respectively), while lower were not significantly different. However, the incidence of conduction block at 260 microM lidocaine was significantly lower (16.7% vs. 56.7%; P < 0.05) in vagal myelinated axons. Conclusions Although no difference in sensitivity to the conduction blocking effects of lidocaine could be demonstrated among dorsal root axons, myelinated axons were more sensitive to the conduction velocity slowing effects of lidocaine. This differential effect cannot explain clinical observations of differential nerve block. Differential sensory block with lidocaine may depend on factors (e.g., physiologic function) related only indirectly to individual axon conduction velocity (diameter).
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Mohan, Suresh, Iván Coto Hernández, Martin K. Selig, Shinsuke Shibata, and Nate Jowett. "Stain-Free Resolution of Unmyelinated Axons in Transgenic Mice Using Fluorescence Microscopy." Journal of Neuropathology & Experimental Neurology 78, no. 12 (September 23, 2019): 1178–80. http://dx.doi.org/10.1093/jnen/nlz099.
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Abstract Though unmyelinated fibers predominate axon counts within peripheral nerves, they are frequently excluded in histomorphometric assessment as they cannot be readily resolved by light microscopy. Herein, we demonstrate stain-free resolution of unmyelinated axons in Sox10-Venus mice by widefield fluorescence imaging of sciatic nerve cryosections. Optional staining of cryosections using a rapid and nontoxic myelin-specific dye (FluoroMyelin Red) enables robust synchronous resolution of myelinated and unmyelinated fibers, comprising a high-throughput platform for neural histomorphometry.
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Graham, B., and S. Redman. "A simulation of action potentials in synaptic boutons during presynaptic inhibition." Journal of Neurophysiology 71, no. 2 (February 1, 1994): 538–49. http://dx.doi.org/10.1152/jn.1994.71.2.538.
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1. During presynaptic inhibition, an increased conductance in the membrane of the presynaptic bouton is presumed to reduce the action potential, thereby reducing transmitter release. The object of the simulation has been to determine the magnitude of a chloride conductance required to reduce transmitter release, for various diameters of synaptic boutons, connected to axons with diameters in the range 0.1-1.0 microns. 2. A propagating action potential was simulated in axons connected to either side of a hemispherical bouton. The axons could be myelinated or unmyelinated, while the bouton membrane could be passive, a node of the myelinated nerve, or have the same active properties as the attached unmyelinated nerve. Membrane properties of the axons were derived from mammalian data and scaled to 37 degrees C. 3. A steady-state chloride conductance was included in the bouton membrane, with ECl = -40 mV. The amplitude of the action potential in the bouton was calculated for different diameters of axon and bouton and for different magnitudes of chloride conductance. 4. Using published data on the relationship between the amplitude of a presynaptic action potential and the resulting postsynaptic potential, the relationship between the chloride conductance and the postsynaptic response was calculated for different geometries. Transmitter release was reduced when an action potential was 90 mV or smaller, with no transmission for action potentials smaller than 50 mV. 5. Conductance increases in the range 3 to 10 nS were required to reduce the action potential to 90 mV, depending on the diameter of the axon (0.5-1.0 microns), diameter of the bouton (3-6 microns), whether the bouton had passive or active membrane, and whether the axon was myelinated or unmyelinated. A 3 microns passive bouton connected to a 0.5 micron myelinated axon was most sensitive to the effects of a chloride conductance, while a 6 microns active bouton connected to a 1 micron myelinated nerve was least sensitive to the effects of a chloride conductance. 6. The reduction in the action potential was compared when ECl = -40 mV and when ECl = E(rest) = -80 mV. Inactivation of the sodium conductance by terminal depolarization was the dominant influence on the amplitude of the action potential. 7. Conductances that were sufficient to completely block synaptic transmission at a bouton were insufficient to prevent the spread of the action potential away from that bouton.(ABSTRACT TRUNCATED AT 400 WORDS)
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Dori, Amir, Glenn Lopate, Rati Choksi, and Alan Pestronk. "Myelinated and unmyelinated endoneurial axon quantitation and clinical correlation." Muscle & Nerve 53, no. 2 (August 8, 2015): 198–204. http://dx.doi.org/10.1002/mus.24740.
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Ye, Hui, and Jeffrey Ng. "Shielding effects of myelin sheath on axolemma depolarization under transverse electric field stimulation." PeerJ 6 (December 3, 2018): e6020. http://dx.doi.org/10.7717/peerj.6020.
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Axonal stimulation with electric currents is an effective method for controlling neural activity. An electric field parallel to the axon is widely accepted as the predominant component in the activation of an axon. However, recent studies indicate that the transverse component to the axolemma is also effective in depolarizing the axon. To quantitatively investigate the amount of axolemma polarization induced by a transverse electric field, we computed the transmembrane potential (Vm) for a conductive body that represents an unmyelinated axon (or the bare axon between the myelin sheath in a myelinated axon). We also computed the transmembrane potential of the sheath-covered axonal segment in a myelinated axon. We then systematically analyzed the biophysical factors that affect axonal polarization under transverse electric stimulation for both the bare and sheath-covered axons. Geometrical patterns of polarization of both axon types were dependent on field properties (magnitude and field orientation to the axon). Polarization of both axons was also dependent on their axolemma radii and electrical conductivities. The myelin provided a significant “shielding effect” against the transverse electric fields, preventing excessive axolemma depolarization. Demyelination could allow for prominent axolemma depolarization in the transverse electric field, via a significant increase in myelin conductivity. This shifts the voltage drop of the myelin sheath to the axolemma. Pathological changes at a cellular level should be considered when electric fields are used for the treatment of demyelination diseases. The calculated term for membrane polarization (Vm) could be used to modify the current cable equation that describes axon excitation by an external electric field to account for the activating effects of both parallel and transverse fields surrounding the target axon.
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Jia, Zelin, and Yinyun Li. "A possible mechanism for neurofilament slowing down in myelinated axon: Phosphorylation-induced variation of NF kinetics." PLOS ONE 16, no. 3 (March 12, 2021): e0247656. http://dx.doi.org/10.1371/journal.pone.0247656.
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Neurofilaments(NFs) are the most abundant intermediate filaments that make up the inner volume of axon, with possible phosphorylation on their side arms, and their slow axonal transport by molecular motors along microtubule tracks in a “stop-and-go” manner with rapid, intermittent and bidirectional motion. The kinetics of NFs and morphology of axon are dramatically different between myelinate internode and unmyelinated node of Ranvier. The NFs in the node transport as 7.6 times faster as in the internode, and the distribution of NFs population in the internode is 7.6 folds as much as in the node of Ranvier. We hypothesize that the phosphorylation of NFs could reduce the on-track rate and slow down their transport velocity in the internode. By modifying the ‘6-state’ model with (a) an extra phosphorylation kinetics to each six state and (b) construction a new ‘8-state’ model in which NFs at off-track can be phosphorylated and have smaller on-track rate, our model and simulation demonstrate that the phosphorylation-induced decrease of on-track rate could slow down the NFs average velocity and increase the axonal caliber. The degree of phosphorylation may indicate the extent of velocity reduction. The Continuity equation used in our paper predicts that the ratio of NFs population is inverse proportional to the ratios of average velocity of NFs between node of Ranvier and internode. We speculate that the myelination of axon could increase the level of phosphorylation of NF side arms, and decrease the possibility of NFs to get on-track of microtubules, therefore slow down their transport velocity. In summary, our work provides a potential mechanism for understanding the phosphorylation kinetics of NFs in regulating their transport and morphology of axon in myelinated axons, and the different kinetics of NFs between node and internode.
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Waxman, Stephen G., and Joel A. Black. "Unmyelinated and myelinated axon membrane from rat corpus callosum: differences in macromolecular structure." Brain Research 453, no. 1-2 (June 1988): 337–43. http://dx.doi.org/10.1016/0006-8993(88)90174-6.
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Einheber, Steven, George Zanazzi, William Ching, Steven Scherer, Teresa A. Milner, Elior Peles, and James L. Salzer. "The Axonal Membrane Protein Caspr, a Homologue of Neurexin IV, Is a Component of the Septate-like Paranodal Junctions That Assemble during Myelination." Journal of Cell Biology 139, no. 6 (December 15, 1997): 1495–506. http://dx.doi.org/10.1083/jcb.139.6.1495.
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We have investigated the potential role of contactin and contactin-associated protein (Caspr) in the axonal–glial interactions of myelination. In the nervous system, contactin is expressed by neurons, oligodendrocytes, and their progenitors, but not by Schwann cells. Expression of Caspr, a homologue of Neurexin IV, is restricted to neurons. Both contactin and Caspr are uniformly expressed at high levels on the surface of unensheathed neurites and are downregulated during myelination in vitro and in vivo. Contactin is downregulated along the entire myelinated nerve fiber. In contrast, Caspr expression initially remains elevated along segments of neurites associated with nascent myelin sheaths. With further maturation, Caspr is downregulated in the internode and becomes strikingly concentrated in the paranodal regions of the axon, suggesting that it redistributes from the internode to these sites. Caspr expression is similarly restricted to the paranodes of mature myelinated axons in the peripheral and central nervous systems; it is more diffusely and persistently expressed in gray matter and on unmyelinated axons. Immunoelectron microscopy demonstrated that Caspr is localized to the septate-like junctions that form between axons and the paranodal loops of myelinating cells. Caspr is poorly extracted by nonionic detergents, suggesting that it is associated with the axon cytoskeleton at these junctions. These results indicate that contactin and Caspr function independently during myelination and that their expression is regulated by glial ensheathment. They strongly implicate Caspr as a major transmembrane component of the paranodal junctions, whose molecular composition has previously been unknown, and suggest its role in the reciprocal signaling between axons and glia.
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Brown, Danielle L., Michael Staup, and Cynthia Swanson. "Stereology of the Peripheral Nervous System." Toxicologic Pathology 48, no. 1 (June 20, 2019): 37–48. http://dx.doi.org/10.1177/0192623319854746.
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Qualitative histopathology has been the gold standard for evaluation of morphological tissue changes in all organ systems, including the peripheral nervous system. However, the human eye is not sensitive enough to detect small changes in quantity or size. Peripheral nervous system toxicity can manifest as subtle changes in neuron size, neuron number, axon size, number of myelinated or unmyelinated axons, or number of nerve fibers. Detection of these changes may be beyond the sensitivity of the human eye alone, necessitating quantitative approaches in some cases. Although 2-dimensional (2D) histomorphometry can provide additional information and is more sensitive than qualitative evaluation alone, the results are not always representative of the entire tissue and assumptions about the tissue can lead to bias, or inaccuracies, in the data. Design-based stereology provides 3D estimates of number, volume, surface area, or length, and stereological principles can be applied to peripheral nervous system tissues to obtain accurate and precise estimates, such as neuron number and size, axon number, and total intraepidermal nerve fiber length. This review describes practical stereological approaches to 3 compartments of the peripheral nervous system: ganglia, peripheral nerves, and intraepidermal nerve fibers.
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Dietz, Friederike B., and Richard A. Jaffe. "Bupivacaine Preferentially Blocks Ventral Root Axons in Rats." Anesthesiology 86, no. 1 (January 1, 1997): 172–80. http://dx.doi.org/10.1097/00000542-199701000-00021.
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Background Clinically, bupivacaine can provide excellent sensory anesthesia with minimal impairment of motor function. However, the mechanisms by which local anesthetics produce differential sensory-motor nerve block is still unknown. The primary site of action for spinal and epidural anesthetics is thought to be the intradural segment of the spinal root. To determine the differential susceptibility of single motor and sensory nerve fibers to local anesthetic conduction block, bupivacaine effects on individual dorsal root (DR) and ventral root (VR) axons were studied. Methods Lumbar DRs and VRs were excised from anesthetized adult male rats. Single-fiber dissection and recording techniques were used to isolate activity in individual axons. Supramaximal constant-voltage stimuli at 0.3 Hz were delivered to the root. During in vitro perfusion, each root was exposed to increasing concentrations of bupivacaine, and the minimum blocking concentration (C(m)) and the concentration that increased conduction latency by 50% (latency EC50) were measured. Results Ventral root axons were significantly more sensitive to the steady-state conduction blocking effects of bupivacaine than were either myelinated or unmyelinated DR axons (DR-C(m), 32.4 microM; VR-C(m), 13.8 microM; P < 0.0001). In addition, VR axons were more susceptible to the latency-increasing effects of bupivacaine than were DR axons (DR-EC50 = 20.7 microM; VR-EC50 = 8.5 microM; P < 0.0001). Within axon groups, differential sensitivity as a function of conduction velocity (axon diameter), or length of nerve exposed to the anesthetic could not be demonstrated. Conclusions In contrast to clinical expectations, low concentrations of bupivacaine preferentially block motor (VR) axons in the rat.
Dissertations / Theses on the topic "Myelinated / Unmyelinated axon"
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Zeng, Shangyou. "Spatial distribution and function of ion channels on neural axon." Ohio : Ohio University, 2005. http://www.ohiolink.edu/etd/view.cgi?ohiou1113855357.
Full textBooks on the topic "Myelinated / Unmyelinated axon"
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Mason, Peggy. Electrical Communication Within a Neuron. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0010.
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Postsynaptic potentials integrate across time and space within a single neuron. The influence of the length constant on spatial summation and of the time constant on temporal summation is described. Whereas passive properties give rise to graded potentials, the voltage-gated sodium channel (VGSC) supports the all-or-none action potential. The action potential can be used to conduct information across long distances and is therefore used in the majority of neurons that have axons. How the inactivated state of VGSCs gives rise to the refractory period and dynamic polarization is described. The meaning of the action potential threshold is fully considered and then applied to understand the clinical condition of hyperkalemic periodic paralysis. Trains of action potentials carry information, and degradation of the spike train compromises the message. The speed of action potential conduction along both unmyelinated and myelinated axons is explored. In closing, an overview of demyelinating diseases is offered.
Book chapters on the topic "Myelinated / Unmyelinated axon"
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Reina, Miguel Angel, Riánsares Arriazu Navarro, and Esther M. Durán Mateos. "Ultrastructure of Myelinated and Unmyelinated Axons." In Atlas of Functional Anatomy for Regional Anesthesia and Pain Medicine, 3–18. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09522-6_1.
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Reeves, Thomas M., Adele E. Doperalski, and Linda L. Phillips. "Unmyelinated and Myelinated Axons Exhibit Differential Injury and Treatment Responses Following Traumatic Injury." In White Matter Injury in Stroke and CNS Disease, 321–72. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9123-1_15.
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Benarroch, Eduardo E. "Peripheral and Spinal Mechanisms of Nociception." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 655–73. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0035.
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Pain is a conscious subjective experience driven by activity of nociceptors. Pain includes not only nociception but also abnormal transmission and processing of painful stimuli. Nociception involves unmyelinated and small myelinated fibers from small dorsal root ganglion neurons that respond to noxious heat, mechanical, or chemically stimuli. These neurons are functional and biochemically heterogeneous in terms of their sensitivity to stimuli, type of afferent axons, neurochemical composition, and targets in the dorsal horn. They activate both second-order projection neurons and different subsets of excitatory and inhibitory interneurons that have a major role in processing of sensory information. Mutations affecting ion channels in nociceptors, inflammatory mediators, or peripheral nerve injury trigger changes and expression of ion channels and receptors. This results in increased excitability of nociceptors, known as peripheral sensitization. Abnormal activity in nociceptors triggers plastic channels in the dorsal horn resulting in altered balance between excitation and inhibition, resulting in central sensitization. Local activation of microglia and astrocytes plays a major role in this process. Elucidation of mechanisms of peripheral and central sensitization provide insight into the pathophysiology of neuropathic pain and potential therapeutic targets for its treatment.
Conference papers on the topic "Myelinated / Unmyelinated axon"
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Pelot, Nicole A., Christina E. Behrend, and Warren M. Grill. "Modeling the response of small myelinated and unmyelinated axons to kilohertz frequency signals." In 2015 7th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2015. http://dx.doi.org/10.1109/ner.2015.7146645.
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Chang, Wesley C., Christopher G. Keller, and David W. Sretavan. "Precision MEMS Nano-Cutting Device for Cellular Microsurgery." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61670.
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An important tool for biological research and microsurgery is a microdevice for the cutting and isolation of subcellular neuronal components such as axons and dendrites for analysis or microsurgery. We have fabricated an easy-to-use, inexpensive and robust MEMS device with a nanoscale cutting tool that performs highly reproducible cutting of axons and dendrites. The device consists of a knife with an 20 nm-sharp edge ranging from 10–200 microns in length and is formed from molding conformally deposited silicon nitride over a potassium hydroxide-etched trench in <100>-oriented single crystal silicon. Knife surfaces are coated with a thin layer of liquid perfluorinated polyether to prevent adhesion of debris from cut targets. The knife is assembled onto a microfabricated suspension and frame consisting of serpentine flexures of single crystal silicon. These supporting structures help to properly orient the knife and control cutting force. We have used this assembled nano-cutting device to make reliable cuts of individual living dendrites and unmyelinated and myelinated axons from both adult and embryonic animal tissue. The cutting device was able to target and cut specific cell processes within a complex field and without disturbing surrounding structures. The cuts were sharp and repeatable, and microdevice’s performance was undiminished with repeated use.