To see the other types of publications on this topic, follow the link: Myelinated / Unmyelinated axon.
Journal articles on the topic 'Myelinated / Unmyelinated axon'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Myelinated / Unmyelinated axon.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
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.
Full textAbstract:
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).
2
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.
Full textAbstract:
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.
3
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.
Full textAbstract:
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)
4
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.
Full text
5
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.
Full textAbstract:
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.
6
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.
Full textAbstract:
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.
7
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.
Full text
8
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.
Full textAbstract:
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.
9
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.
Full textAbstract:
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.
10
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.
Full textAbstract:
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.
11
Davis, J. Q., S. Lambert, and V. Bennett. "Molecular composition of the node of Ranvier: identification of ankyrin-binding cell adhesion molecules neurofascin (mucin+/third FNIII domain-) and NrCAM at nodal axon segments." Journal of Cell Biology 135, no. 5 (December 1, 1996): 1355–67. http://dx.doi.org/10.1083/jcb.135.5.1355.
Full textAbstract:
Neurofascin, NrCAM, L1, and NgCAM are a family of Ig/FNIII cell adhesion molecules that share ankyrin-binding activity in their cytoplasmic domains, and are candidates to form membrane-spanning complexes with members of the ankyrin family of spectrin-binding proteins in a variety of cellular contexts in the nervous system. Specialized forms of ankyrin, 270 kD and/or 480 kD ankyrinG are components of the membrane undercoat of axons at the node of Ranvier. This paper focuses on definition of the isoforms of ankyrin-binding cell adhesion molecules localized with ankyrinG at the nodal axon segment. The exon usage of two major forms of neurofascin was determined by isolation of full-length cDNAs and used to prepare isoform-specific antibodies. An isoform of neurofascin containing a mucin-like domain and lacking the third FNIII domain was concentrated at axon initial segments and colocalized at nodes of Ranvier with ankyrinG and the voltage-dependent sodium channel. An alternative form of neurofascin lacking the mucin-like domain and containing the third FNIII domain was present in unmyelinated axons. The antibody initially raised against neurofascin was used to screen a rat brain cDNA expression library. In addition to neurofascin, this screen yielded a clone with 80% sequence identity to NrCAM from chicken. The sequences of two full-length cDNAs are presented. NrCAM is most closely related to neurofascin among the other members of the L1/neurofascin/NgCAM family, with over 70% identity between cytoplasmic domains. NrCAM, visualized with antibodies specific for the ecto-domain, also was found to be coexpressed with neurofascin at nodes of Ranvier and at axon initial segments. This is the first characterization of defined neuronal cell adhesion molecules localized to axonal membranes at the node of Ranvier of myelinated axons.
12
Camilieri-Asch, Victoria, Kara E. Yopak, Alethea Rea, Jonathan D. Mitchell, Julian C. Partridge, and Shaun P. Collin. "Convergence of Olfactory Inputs within the Central Nervous System of a Cartilaginous and a Bony Fish: An Anatomical Indicator of Olfactory Sensitivity." Brain, Behavior and Evolution 95, no. 3-4 (2020): 139–61. http://dx.doi.org/10.1159/000510688.
Full textAbstract:
The volume of the olfactory bulbs (OBs) relative to the brain has been used previously as a proxy for olfactory capabilities in many vertebrate taxa, including fishes. Although this gross approach has predictive power, a more accurate assessment of the number of afferent olfactory inputs and the convergence of this information at the level of the telencephalon is critical to our understanding of the role of olfaction in the behaviour of fishes. In this study, we used transmission electron microscopy to assess the number of first-order axons within the olfactory nerve (ON) and the number of second-order axons in the olfactory peduncle (OP) in established model species within cartilaginous (brownbanded bamboo shark, <i>Chiloscyllium punctatum</i> [CP]) and bony (common goldfish, <i>Carassius auratus</i> [CA]) fishes. The total number of axons varied from a mean of 18.12 ± 7.50 million in the ON to a mean of 0.38 ± 0.21 million in the OP of CP, versus 0.48 ± 0.16 million in the ON and 0.09 ± 0.02 million in the OP of CA. This resulted in a convergence ratio of approximately 50:1 and 5:1, respectively, for these two species. Based on astroglial ensheathing, axon type (unmyelinated [UM] and myelinated [M]) and axon size, we found no differentiated tracts in the OP of CP, whereas a lateral and a medial tract (both of which could be subdivided into two bundles or areas) were identified for CA, as previously described. Linear regression analyses revealed significant differences not only in axon density between species and locations (nerves and peduncles), but also in axon type and axon diameter (<i>p</i> < 0.05). However, UM axon diameter was larger in the OPs than in the nerve in both species (<i>p</i> = 0.005), with no significant differences in UM axon diameter in the ON (<i>p</i> = 0.06) between species. This study provides an in-depth analysis of the neuroanatomical organisation of the ascending olfactory pathway in two fish taxa and a quantitative anatomical comparison of the summation of olfactory information. Our results support the assertion that relative OB volume is a good indicator of the level of olfactory input and thereby a proxy for olfactory capabilities.
13
Lubba, Carl H., Yann Le Guen, Sarah Jarvis, Nick S. Jones, Simon C. Cork, Amir Eftekhar, and Simon R. Schultz. "PyPNS: Multiscale Simulation of a Peripheral Nerve in Python." Neuroinformatics 17, no. 1 (June 15, 2018): 63–81. http://dx.doi.org/10.1007/s12021-018-9383-z.
Full textAbstract:
Abstract Bioelectronic Medicines that modulate the activity patterns on peripheral nerves have promise as a new way of treating diverse medical conditions from epilepsy to rheumatism. Progress in the field builds upon time consuming and expensive experiments in living organisms. To reduce experimentation load and allow for a faster, more detailed analysis of peripheral nerve stimulation and recording, computational models incorporating experimental insights will be of great help. We present a peripheral nerve simulator that combines biophysical axon models and numerically solved and idealised extracellular space models in one environment. We modelled the extracellular space as a three-dimensional resistive continuum governed by the electro-quasistatic approximation of the Maxwell equations. Potential distributions were precomputed in finite element models for different media (homogeneous, nerve in saline, nerve in cuff) and imported into our simulator. Axons, on the other hand, were modelled more abstractly as one-dimensional chains of compartments. Unmyelinated fibres were based on the Hodgkin-Huxley model; for myelinated fibres, we adapted the model proposed by McIntyre et al. in 2002 to smaller diameters. To obtain realistic axon shapes, an iterative algorithm positioned fibres along the nerve with a variable tortuosity fit to imaged trajectories. We validated our model with data from the stimulated rat vagus nerve. Simulation results predicted that tortuosity alters recorded signal shapes and increases stimulation thresholds. The model we developed can easily be adapted to different nerves, and may be of use for Bioelectronic Medicine research in the future.
14
Chakrabarty, Anuradha, Audrey Blacklock, Stanislav Svojanovsky, and Peter G. Smith. "Estrogen Elicits Dorsal Root Ganglion Axon Sprouting via a Renin-Angiotensin System." Endocrinology 149, no. 7 (April 3, 2008): 3452–60. http://dx.doi.org/10.1210/en.2008-0061.
Full textAbstract:
Many painful conditions occur more frequently in women, and estrogen is a predisposing factor. Estrogen may contribute to some pain syndromes by enhancing axon outgrowth by sensory dorsal root ganglion (DRG) neurons. The objective of the present study was to define mechanisms by which estrogen elicits axon sprouting. The estrogen receptor-α agonist propyl pyrazole triol induced neurite outgrowth from cultured neonatal DRG neurons, whereas the estrogen receptor-β agonist diarylpropionitrile was ineffective. 17β-Estradiol (E2) elicited sprouting from peripherin-positive unmyelinated neurons, but not larger NF200-positive myelinated neurons. Microarray analysis showed that E2 up-regulates angiotensin II (ANGII) receptor type 2 (AT2) mRNA in vitro, and studies in adult rats confirmed increased DRG mRNA and protein in vivo. AT2 plays a central role in E2-induced axon sprouting because AT2 blockade by PD123,319 eliminated estrogen-mediated sprouting in vitro. We assessed whether AT2 may be responding to locally synthesized ANGII. DRG from adult rats expressed mRNA for renin, angiotensinogen, and angiotensin converting enzyme (ACE), and protein products were present and occasionally colocalized within neurons and other DRG cells. We determined if locally synthesized ANGII plays a role in estrogen-mediated sprouting by blocking its formation using the ACE inhibitor enalapril. ACE inhibition prevented estrogen-induced neuritogenesis. These findings support the hypothesis that estrogen promotes DRG nociceptor axon sprouting by up-regulating the AT2 receptor, and that locally synthesized ANGII can induce axon formation. Therefore, estrogen may contribute to some pain syndromes by enhancing the pro-neuritogenic effects of AT2 activation by ANGII.
15
Hijazi, Mido M., Sylvia J. Buchmann, Annahita Sedghi, Ben M. Illigens, Heinz Reichmann, Gabriele Schackert, and Timo Siepmann. "Assessment of cutaneous axon-reflex responses to evaluate functional integrity of autonomic small nerve fibers." Neurological Sciences 41, no. 7 (March 3, 2020): 1685–96. http://dx.doi.org/10.1007/s10072-020-04293-w.
Full textAbstract:
Abstract Cutaneous autonomic small nerve fibers encompass unmyelinated C-fibers and thinly myelinated Aδ-fibers, which innervate dermal vessels (vasomotor fibers), sweat glands (sudomotor fibers), and hair follicles (pilomotor fibers). Analysis of their integrity can capture early pathology in autonomic neuropathies such as diabetic autonomic neuropathy or peripheral nerve inflammation due to infectious and autoimmune diseases. Furthermore, intraneural deposition of alpha-synuclein in synucleinopathies such as Parkinson’s disease can lead to small fiber damage. Research indicated that detection and quantitative analysis of small fiber pathology might facilitate early diagnosis and initiation of treatment. While autonomic neuropathies show substantial etiopathogenetic heterogeneity, they have in common impaired functional integrity of small nerve fibers. This impairment can be evaluated by quantitative analysis of axonal responses to iontophoretic application of adrenergic or cholinergic agonists to the skin. The axon-reflex can be elicited in cholinergic sudomotor fibers to induce sweating and in cholinergic vasomotor fibers to induce vasodilation. Currently, only few techniques are available to quantify axon-reflex responses, the majority of which is limited by technical demands or lack of validated analysis protocols. Function of vasomotor small fibers can be analyzed using laser Doppler flowmetry, laser Doppler imaging, and laser speckle contrast imaging. Sudomotor function can be assessed using quantitative sudomotor axon-reflex test, silicone imprints, and quantitative direct and indirect testing of sudomotor function. More recent advancements include analysis of piloerection (goose bumps) following stimulation of adrenergic small fibers using pilomotor axon-reflex test. We provide a review of the current literature on axon-reflex tests in cutaneous autonomic small fibers.
16
CEBALLOS, DOLORES, JORDI CUADRAS, ENRIQUE VERDÚ, and XAVIER NAVARRO. "Morphometric and ultrastructural changes with ageing in mouse peripheral nerve." Journal of Anatomy 195, no. 4 (November 1999): 563–76. http://dx.doi.org/10.1017/s0021878299005610.
Full textAbstract:
Qualitative and quantitative information is reported on the morphological changes that occur in nerve fibres and nonneuronal cells of peripheral nerve during the lifetime of the mouse. Tibial nerves of mice aged 6–33 mo were studied. With ageing, collagen accumulates in the perineurium and lipid droplets in the perineurial cells. Macrophages and mast cells increase in number, and onion bulbs and collagen pockets are frequently present. Schwann cells associated with myelinated fibres (MF) slightly decrease in number in parallel with an increase of the internodal length from 6 to 12 mo, but increase in older nerves when demyelination and remyelination are common. The unmyelinated axon to myelinated fibre (UA/MF) ratio was about 2 until 12 mo, decreasing to 1.6 by 27 mo. In older mice, the loss of nerve fibres involves UA (50% loss of 27–33 mo cf. 6 mo) more markedly than MF (35%). In aged nerves wide incisures and infolded or outfolded myelin loops are frequent, resulting in an increased irregularity in the morphology of fibres along the internodes. In the mouse there is an adult time period, 12–20 mo, during which several features of degeneration progressively appear, and an ageing period from 20 mo upwards when the nerve suffers a general disorganisation and marked fibre loss.
17
Kimball, Elizabeth, Julie Schaub, Sarah Quillen, Casey Keuthan, Mary Ellen Pease, Arina Korneva, and Harry Quigley. "The role of aquaporin-4 in optic nerve head astrocytes in experimental glaucoma." PLOS ONE 16, no. 2 (February 2, 2021): e0244123. http://dx.doi.org/10.1371/journal.pone.0244123.
Full textAbstract:
Purpose To study aquaporin channel expression in astrocytes of the mouse optic nerve (ON) and the response to IOP elevation in mice lacking aquaporin 4 (AQP4 null). Methods C57BL/6 (B6) and AQP4 null mice were exposed to bead-induced IOP elevation for 3 days (3D-IOP), 1 and 6 weeks. Mouse ocular tissue sections were immunolabeled against aquaporins 1(AQP1), 4(AQP4), and 9(AQP9). Ocular tissue was imaged to identify normal AQP distribution, ON changes, and axon loss after IOP elevation. Ultrastructure examination, cell proliferation, gene expression, and transport block were also analyzed. Results B6 mice had abundant AQP4 expression in Müller cells, astrocytes of retina and myelinated ON (MON), but minimal AQP4in prelaminar and unmyelinated ON (UON). MON of AQP4 nulls had smaller ON area, smaller axon diameter, higher axon density, and larger proportionate axon area than B6 (all p≤0.05). Bead-injection led to comparable 3D-IOP elevation (p = 0.42) and axonal transport blockade in both strains. In B6, AQP4 distribution was unchanged after 3D-IOP. At baseline, AQP1 and AQP9 were present in retina, but not in UON and this was unaffected after IOP elevation in both strains. In 3D-IOP mice, ON astrocytes and microglia proliferated, more in B6 than AQP4 null. After 6 week IOP elevation, axon loss occurred equally in the two mouse types (24.6%, AQP4 null vs. 23.3%, B6). Conclusion Lack of AQP4 was neither protective nor detrimental to the effects of IOP elevation. The minimal presence of AQP4 in UON may be a vital aspect of the regionally specific phenotype of astrocytes in the mouse optic nerve head.
18
Wong-Riley, Margaret T. T., Thomas C. Trusk, Satish C. Tripathi, and Daniel A. Hoppe. "Effect of retinal impulse blockage on cytochrome oxidase-rich zones in the macaque striate cortex: II. Quantitative electron-microscopic (EM) analysis of neuropil." Visual Neuroscience 2, no. 5 (May 1989): 499–514. http://dx.doi.org/10.1017/s0952523800012396.
Full textAbstract:
AbstractUnilateral retinal impulse blockage with tetrodotoxin (TTX) induces reversible shrinkage and decreased cytochrome oxidase (CO) activity in alternate rows of supragranular, CO-rich puffs in the adult macaque striate cortex (Wong-Riley & Carroll, 1984b: Carroll & Wong-Riley, 1987). The present study extended the findings to the electron-microscopic (EM) level to determine if various neuropil profiles in control puffs exhibit heterogeneous levels of CO activity, and whether specific processes were more susceptible to intravitreal TTX than others.Within the neuropil of control puffs, 60% of the total mitochondrial population resided in dendrites, and the majority of dendritic mitochondria were highly reactive for CO. Axon terminals forming symmetrical synapses also contained darkly reactive mitochondria, whereas those forming asymmetrical synapses possessed very few and mainly lightly reactive mitochondria. Unmyelinated axon trunks, myelinated axons, and glia all exhibited low levels of CO activity. Synaptic count revealed a 3:1 ratio of asymmetrical to symmetrical synapses.Intravitreal TTX for 2–4 weeks adversely affects dendrites and symmetrical terminals much more so than other neuropil processes. There was a general decrease in darkly and moderately reactive mitochondria and an increase in lightly reactive mitochondria throughout the puffs, especially in dendrites. This indicates that afferent blockade is more detrimental to processes of higher metabolic activity. Changes also differed between central and peripheral regions of puffs, and indications of axonal and synaptic reorganization were more evident in the latter. Thus, stabilization of neuronal structure and synapses appears to be activity-dependent even in the adult. A working model of these metabolic and morphological responses to chronic TTX is proposed.
19
Carter, Deborah A., and S. J. W. Lisney. "Changes in myelinated and unmyelinated axon numbers in the proximal parts of rat sural nerves after two types of injury." Restorative Neurology and Neuroscience 3, no. 2 (1991): 65–73. http://dx.doi.org/10.3233/rnn-1991-3203.
Full text
20
Dietz, Friederike B., and Richard A. Jaffe. "Pregnancy Does Not Increase Susceptibility to Bupivacaine in Spinal Root Axons." Anesthesiology 87, no. 3 (September 1, 1997): 610–16. http://dx.doi.org/10.1097/00000542-199709000-00022.
Full textAbstract:
Background The underlying mechanism of enhanced antinociceptive effects and increased susceptibility to local anesthetics during pregnancy is not known. Mechanical, hormonal, biochemical, and neural changes have been suggested. The authors measured the susceptibility of individual spinal root axons to bupivacaine during late pregnancy in rats and compared them with similar measurements in nonpregnant rats. Methods Lumbar dorsal and ventral roots were excised from anesthetized pregnant and nonpregnant rats. Single-fiber dissection and recording techniques were used to isolate activity in individual axons. Supramaximal constant voltage stimuli were delivered to the distal end of the root. During in vitro perfusion, each root was exposed to increasing concentrations of bupivacaine, and the minimum blocking concentration (Cm) and the concentration that increased conduction latency by 50% (EC50) were measured. Results Myelinated and unmyelinated dorsal and ventral root axons of pregnant rats appeared to be less sensitive to steady-state conduction block and to the latency-increasing effects of bupivacaine than were equivalent axons from nonpregnant rats. Although when comparing specific axon types, only the difference in C-fibers was significant (Cm = 29.8 microM for pregnant and Cm = 22.1 microM for nonpregnant rats, P < 0.05; EC50 = 19.9 microM and 13.6 microM, respectively). Conclusions In contrast to clinical expectations, the susceptibility to bupivacaine conduction block in individual dorsal and ventral root axons during late pregnancy in rats was not greater in pregnant animals. Pregnancy-related changes in diffusion barriers and activation of endogenous analgesic systems without changes in the electrophysiologic properties of spinal root axons are suggested as possible explanations for the discrepancy between clinical and experimental observations.
21
Gregory, J. E., and U. Proske. "Fusimotor axons in the kitten." Journal of Neurophysiology 56, no. 5 (November 1, 1986): 1462–73. http://dx.doi.org/10.1152/jn.1986.56.5.1462.
Full textAbstract:
In kittens 1- to 23-days old growth of axons in the soleus nerve has been studied using the structural parameters nerve length, internodal length, and axonal diameter. In addition, single functional fusimotor axons were isolated in lumbosacral ventral roots, and the responses of muscle spindles in soleus were studied during fusimotor stimulation. While nerve length over the soleus nerve to lumbar spinal root increased from 41 to 76 mm during the 22 days, mean internodal length increased from 250 to 410 microns. Mean axon diameter increased from 2.1 to 4.1 microns. In the youngest animals values for both internodal length and axon diameter were distributed uniformly about the mean. From day 11 onward the distributions became bimodal, including a growing number of new axons in the small-myelinated range. Filaments of ventral root were isolated that on repetitive stimulation had a specific excitatory effect on the discharge of muscle spindles. The responses could be attributed to axons that were not associated with measurable tension and were therefore likely to be fusimotor fibers. Measurements of the conduction velocity of skeletomotor and fusimotor axons showed that conduction speed increased progressively with age for both groups, but the rate of increase was more than three times faster in the most rapidly conducting skeletomotor axons compared with the fusimotor axons. The distribution of conduction velocities for fusimotor fibers showed two peaks, one in the range typical for conduction in unmyelinated fibers, 0.5-1.0 m/s, the second at 3-4 m/s. The small number of values in the range of 1-2 m/s was attributed to the process of myelination. It is suggested that conduction speed increases discontinuously over this part of the range as impulse conduction changes from continuous propagation to saltatory transmission. Eighteen fusimotor axons could be classified as having either a static or a dynamic action on spindle discharge. Repetitive stimulation of fusimotor fibers during a ramp-and-hold stretch of the muscle produced a characteristic response. Fibers classified as dynamic had little effect on the response of the spindle when the muscle was held at a particular length but greatly increased the response during a length change. Static fusimotor fibers, on stimulation, increased the response of the spindle at constant length but did not evoke a selective increase during the length change. Both kinds of fusimotor effects were characterized by overall low firing rates.
22
WALKER, DAVID, ANNE CARRINGTON, SUSAN A. CANNAN, DIANE SAWICKI, JANET SREDY, ANDREW J. M. BOULTON, and RAYAZ A. MALIK. "Structural abnormalities do not explain the early functional abnormalities in the peripheral nerves of the streptozotocin diabetic rat." Journal of Anatomy 195, no. 3 (October 1999): 419–27. http://dx.doi.org/10.1017/s002187829900549x.
Full textAbstract:
The streptozotocin (STZ)-diabetic rat, the most commonly employed model of experimental diabetic neuropathy, is characterised by a reduction in nerve conduction velocity, pain threshold and blood flow. Whether or not structural abnormalities underlie these functional abnormalities is unclear. 10 adult male Sprague–Dawley STZ-diabetic rats (diabetes duration 27 d) and 10 age-matched (23 wk) control animals were studied. Motor nerve conduction velocity (m s−1) was significantly reduced in diabetic (41.31±0.8) compared with control (46.15±1.5) animals (P<0.001). The concentration of sciatic nerve glucose (P<0.001), fructose (P<0.001) and sorbitol (P<0.001) was elevated, and myoinositol (P<0.001) was reduced in diabetic compared with control animals. Detailed morphometric studies demonstrated no significant difference in fascicular area, myelinated fibre density, fibre and axon areas as well as unmyelinated fibre density and diameter. Endoneurial capillary density, basement membrane area and endothelial cell profile number did not differ between diabetic and control animals. However, luminal area (P<0.03) was increased and endothelial cell area (P<0.08) was decreased in the diabetic rats. We conclude there is no detectable structural basis for the reduction in nerve conduction velocity, pain threshold or blood flow, observed in the streptozotocin diabetic rat.
23
Lee, CK, A. Alarfaj, J. Ai, B. Alharbi, P. Vasdev, and RL Macdonald. "Neurosurgery (Neuro Vascular)." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (May 2015): S48. http://dx.doi.org/10.1017/cjn.2015.216.
Full textAbstract:
Background: Blood breakdown products such as bilirubin and bilirubin oxidation products damage cortex and white matter after intracerebral hemorrhage(ICH). Here, we tested whether albumin can antagonize axonal damage caused by bilirubin. Methods: The effect of albumin on white matter injury was investigated using brain slices in vitro. After CD-1 mice brain slices were cut using a vibratome, they were incubated in one of five solutions: artificial cerebral spinal fluid (ACSF), bilirubin ACSF, bilirubin and albumin ACSF, bilirubin ACSF that had albumin added 1 hour(h) later, and bilirubin and denatured albumin ACSF. All solutions were continuously aerated with 95% O2 and 5% CO2. Subsequently, electrophysiological recordings of axonal response to electrical stimulation were performed 8h after incubation of brain slices. Results: Bilirubin treatment profoundly damaged both myelinated and unmeylinated axons in brain slices, but had a greater effect on myelinated axons. Unmyelinated axons were found to be more susceptible to damage from denatured albumin. Albumin treatment at 0 h and 1 h significantly diminished bilirubin toxicity for both myelinated and unmyelinated axons, with 1 h delayed albumin treatment conferring greater neuroprotection. Conclusions: These results implicate the role of albumin in preventing bilirubin-induced axonal damage following ICH and its potential therapeutic value for hemorrhagic stroke.
24
Kordeli, E., J. Davis, B. Trapp, and V. Bennett. "An isoform of ankyrin is localized at nodes of Ranvier in myelinated axons of central and peripheral nerves." Journal of Cell Biology 110, no. 4 (April 1, 1990): 1341–52. http://dx.doi.org/10.1083/jcb.110.4.1341.
Full textAbstract:
Two variants of ankyrin have been distinguished in rat brain tissue using antibodies: a broadly distributed isoform (ankyrinB) that represents the major form of ankyrin in brain and another isoform with a restricted distribution (ankyrinR) that shares epitopes with erythrocyte ankyrin. The ankyrinR isoform was localized by immunofluorescence in cryosections of rat spinal cord gray matter and myelinated central and peripheral nerves to: (a) perikarya and initial axonal segments of neuron cells, (b) nodes of Ranvier of myelinated nerve with no detectable labeling in other areas of the myelinated axons, and (c) the axolemma of unmyelinated axons. Immunogold EM on ultrathin cryosections of myelinated nerve showed that ankyrinR was localized on the cytoplasmic face of the axolemma and was restricted to the nodal and, in some cases, paranodal area. The major isoform of ankyrin in brain (ankyrinB) displayed a broad distribution on glial and neuronal cells of the gray matter and a mainly glial distribution in central myelinated axons with no significant labeling on the axolemma. These results show that (a) ankyrin isoforms display a differential distribution on glial and neuronal cells of the nervous tissue; (b) an isoform of ankyrin codistributes with the voltage-dependent sodium channel in both myelinated and unmyelinated nerve fibers. Ankyrin interacts in vitro with the voltage-dependent sodium channel (Srinivasan, Y., L. Elmer, J. Davis, V. Bennett, and K. Angelides. 1988. Nature (Lond.). 333:177-180). A specific interaction of an isoform of ankyrin with the sodium channel thus may play an important role in the morphogenesis and/or maintenance of the node of Ranvier.
25
Spector, J. Gershon, Albert Derby, Patty Lee, and Dikla G. Roufa. "Comparison of Rabbit Facial Nerve Regeneration in Nerve Growth Factor-Containing Silicone Tubes to that in Autologous Neural Grafts." Annals of Otology, Rhinology & Laryngology 104, no. 11 (November 1995): 875–85. http://dx.doi.org/10.1177/000348949510401110.
Full textAbstract:
Previous reports suggest that nerve growth factor (NGF) enhanced nerve regeneration in rabbit facial nerves. We compared rabbit facial nerve regeneration in 10-mm silicone tubes prefilled with NGF or cytochrome C (Cyt C), bridging an 8-mm nerve gap, to regeneration of 8-mm autologous nerve grafts. Three weeks following implantation, NGF-treated regenerates exhibited a more mature fascicular organization and more extensive neovascularization than Cyt C-treated controls. Morphometric analysis at the middle of the tube of 3- and 5-week regenerates revealed no significant difference in the mean number of myelinated or unmyelinated axons between NGF- and Cyt C-treated implants. However, when the numbers of myelinated fibers in 5-week regenerates were compared to those in their respective preoperative controls, NGF-treated regenerates had recovered a significantly greater percentage of myelinated axons than Cyt C-treated implants (46% versus 18%, respectively). The number of regenerating myelinated axons in the autologous nerve grafts at 5 weeks was significantly greater than the number of myelinated axons in the silicone tubes. However, in the nerve grafts the majority of the axons were found in the extrafascicular connective tissue (66%). The majority of these myelinated fibers did not find their way into the distal nerve stump. Thus, although the number of regenerating myelinated axons within the nerve grafts is greater than that of axons within silicone tube implants, functional recovery of autologous nerve graft repairs may not be superior to that of intubational repairs.
26
Blumer, Roland, Sandra Boesmueller, Bernhard Gesslbauer, Lena Hirtler, Daniel Bormann, Angel M. Pastor, Johannes Streicher, and Rainer Mittermayr. "Structural and molecular characteristics of axons in the long head of the biceps tendon." Cell and Tissue Research 380, no. 1 (December 7, 2019): 43–57. http://dx.doi.org/10.1007/s00441-019-03141-4.
Full textAbstract:
AbstractThe innervation of the long head of the biceps tendon (LHBT) is not sufficiently documented. This is a drawback since pathologies of the LHBT are a major source of shoulder pain. Thus, the study aimed to characterize structurally and molecularly nervous elements of the LHBT. The proximal part of 11 LHBTs was harvested intraoperatively. There were 8 female and 3 male specimens. Age ranged from 66 to 86 years. For structural analyses, nervous elements were viewed in the transmission electron microscope. For molecular characterization, we used general neuronal markers including antibodies against neurofilament and protein gene product 9.5 (PGP9.5) as well as specific neuronal markers including antibodies against myelin basic protein (MBP), calcitonin gene-related product (CGRP), substance P (SP), tyrosine hydroxylase (TH), and growth-associated protein 43 (GAP43). Anti-neurofilament and anti-PGP9.5 visualized the overall innervation. Anti-MBP visualized myelination, anti-CGRP and anti-SP nociceptive fibers, anti-TH sympathetic nerve fibers, and anti-GAP43 nerve fibers during development and regeneration. Immunolabeled sections were analyzed in the confocal laser scanning microscope. We show that the LHBT contains unmyelinated as well as myelinated nerve fibers which group in nerve fascicles and follow blood vessels. Manny myelinated and unmyelinated axons exhibit molecular features of nociceptive nerve fibers. Another subpopulation of unmyelinated axons exhibits molecular characteristics of sympathetic nerve fibers. Unmyelinated sympathetic fibers and unmyelinated nociceptive fibers express proteins that are found during development and regeneration. Present findings support the hypothesis that ingrowth of nociceptive fibers are the source of chronic tendon pain.
27
Dietz, Friederike B., and Richard A. Jaffe. "Indocyanine Green." Anesthesiology 98, no. 2 (February 1, 2003): 516–20. http://dx.doi.org/10.1097/00000542-200302000-00034.
Full textAbstract:
Background The inadvertent intravascular injection of a local anesthetic during epidural anesthesia is an uncommon but potentially serious complication. Epinephrine, the most commonly used marker, does not provide sufficient sensitivity to exclude intravascular injection in all patient populations. The dye indocyanine green (ICG) has been proposed as an alternative marker. It has been demonstrated that ICG could be used to detect intravascular injections with a simple transcutaneous spectrophotometric technique. Although the safety of intravenous ICG is well documented, its neurotoxic potential requires careful study given the probability of inadvertent intrathecal injection during test injections used to verify epidural catheter placement. Methods In this study, the authors investigated the neurophysiologic effects of clinically relevant concentrations of ICG (range, 28.6-286 microm) on single myelinated and unmyelinated dorsal root axons in rats by measuring effects on impulse generation and conduction. Results In contrast to the apparent absence of toxicity when injected intravenously, ICG applied to intact dorsal roots at concentrations likely to be encountered with an epidural test dose produced long-lasting conduction block (21 of 26 axons) or spontaneous bursting activity (7 of 26 axons) in myelinated and unmyelinated dorsal root axons. Conclusion Given this apparent neurotoxicity, ICG should not be used when intrathecal or nerve root injection is possible.
28
Herbin, M., J. P. Rio, J. RepéRant, H. M. Cooper, E. Nevo, and M. Lemire. "Ultrastructural study of the optic nerve in blind mole-rats (Spalacidae, Spalax)." Visual Neuroscience 12, no. 2 (March 1995): 253–61. http://dx.doi.org/10.1017/s0952523800007938.
Full textAbstract:
AbstractThe optic nerve in two species of subterranean mole-rats (Spalacidae) has been examined at the ultrastructural level. The axial length of the eye and the diameter of the optic nerve are 1.9 mm and 52.5 μm in Spalax leucodon, and 0.7 mm and 80.8 μm in Spalax ehrenbergi, respectively. An anti-glial fibrillary acidic protein postembedding procedure was used to distinguish glial cell processes from axons. In both species, the optic nerve is composed exclusively of unmyelinated axons and a spatial distribution gradient according to the size or the density of fibers is lacking. The optic nerve of S. leucodon contains 1790 fibers ranging in diameter from 0.07–2.30 μm (mean = 0.57 μm), whereas in S. ehrenbergi, only 928 fibers, with diameters of 0.04–1.77 μm (mean = 0.53 μm) are observed. In S. ehrenbergi, a higher proportion of glial tissue is present and the fascicular organization of optic fibers is less obvious. Distribution gradients according to size frequency or density of fibers in the optic nerve are absent in both species. Comparison with other mammals suggests that although ocular regression in microphthalmic species is correlated with a significant decrease in the total number of optic fibers and the relative proportion of myelinated fibers, no difference in the absolute size range of unmyelinated axons is observed. The total absence of myelinated fibers in Spalax may be related to the subcutaneous location of the eyes. The unique presence of unmyelinated fibers in the optic nerve is discussed in relation to the possible conservation of a single class of W-like ganglion cells in the retina, in relation to photoperiodic perception.
29
Lakovic, Katarina, Jinglu Ai, Josephine D'Abbondanza, Asma Tariq, Mohammed Sabri, Abdullah K. Alarfaj, Punarjot Vasdev, and Robert Loch Macdonald. "Bilirubin and its Oxidation Products Damage Brain White Matter." Journal of Cerebral Blood Flow & Metabolism 34, no. 11 (August 27, 2014): 1837–47. http://dx.doi.org/10.1038/jcbfm.2014.154.
Full textAbstract:
Brain injury after intracerebral hemorrhage (ICH) occurs in cortex and white matter and may be mediated by blood breakdown products, including hemoglobin and heme. Effects of blood breakdown products, bilirubin and bilirubin oxidation products, have not been widely investigated in adult brain. Here, we first determined the effect of bilirubin and its oxidation products on the structure and function of white matter in vitro using brain slices. Subsequently, we determined whether these compounds have an effect on the structure and function of white matter in vivo. In all, 0.5 mmol/L bilirubin treatment significantly damaged both the function and the structure of myelinated axons but not the unmyelinated axons in brain slices. Toxicity of bilirubin in vitro was prevented by dimethyl sulfoxide. Bilirubin oxidation products (BOXes) may be responsible for the toxicity of bilirubin. In in vivo experiments, unmyelinated axons were found more susceptible to damage from bilirubin injection. These results suggest that unmyelinated axons may have a major role in white-matter damage in vivo. Since bilirubin and BOXes appear in a delayed manner after ICH, preventing their toxic effects may be worth investigating therapeutically. Dimethyl sulfoxide or its structurally related derivatives may have a potential therapeutic value at antagonizing axonal damage after hemorrhagic stroke.
30
Zang, Yunliang, and Eve Marder. "Interactions among diameter, myelination, and the Na/K pump affect axonal resilience to high-frequency spiking." Proceedings of the National Academy of Sciences 118, no. 32 (August 5, 2021): e2105795118. http://dx.doi.org/10.1073/pnas.2105795118.
Full textAbstract:
Axons reliably conduct action potentials between neurons and/or other targets. Axons have widely variable diameters and can be myelinated or unmyelinated. Although the effect of these factors on propagation speed is well studied, how they constrain axonal resilience to high-frequency spiking is incompletely understood. Maximal firing frequencies range from ∼1 Hz to >300 Hz across neurons, but the process by which Na/K pumps counteract Na+ influx is slow, and the extent to which slow Na+ removal is compatible with high-frequency spiking is unclear. Modeling the process of Na+ removal shows that large-diameter axons are more resilient to high-frequency spikes than are small-diameter axons, because of their slow Na+ accumulation. In myelinated axons, the myelinated compartments between nodes of Ranvier act as a “reservoir” to slow Na+ accumulation and increase the reliability of axonal propagation. We now find that slowing the activation of K+ current can increase the Na+ influx rate, and the effect of minimizing the overlap between Na+ and K+ currents on spike propagation resilience depends on complex interactions among diameter, myelination, and the Na/K pump density. Our results suggest that, in neurons with different channel gating kinetic parameters, different strategies may be required to improve the reliability of axonal propagation.
31
Evonuk, Kirsten S., Ryan E. Doyle, Carson E. Moseley, Ian M. Thornell, Keith Adler, Amanda M. Bingaman, Mark O. Bevensee, Casey T. Weaver, Booki Min, and Tara M. DeSilva. "Reduction of AMPA receptor activity on mature oligodendrocytes attenuates loss of myelinated axons in autoimmune neuroinflammation." Science Advances 6, no. 2 (January 2020): eaax5936. http://dx.doi.org/10.1126/sciadv.aax5936.
Full textAbstract:
Glutamate dysregulation occurs in multiple sclerosis (MS), but whether excitotoxic mechanisms in mature oligodendrocytes contribute to demyelination and axonal injury is unexplored. Although current treatments modulate the immune system, long-term disability ensues, highlighting the need for neuroprotection. Glutamate is elevated before T2-visible white matter lesions appear in MS. We previously reported that myelin-reactive T cells provoke microglia to release glutamate from the system xc− transporter promoting myelin degradation in experimental autoimmune encephalomyelitis (EAE). Here, we explore the target for glutamate in mature oligodendrocytes. Most glutamate-stimulated calcium influx into oligodendrocyte somas is AMPA receptor (AMPAR)–mediated, and genetic deletion of AMPAR subunit GluA4 decreased intracellular calcium responses. Inducible deletion of GluA4 on mature oligodendrocytes attenuated EAE and loss of myelinated axons was selectively reduced compared to unmyelinated axons. These data link AMPAR signaling in mature oligodendrocytes to the pathophysiology of myelinated axons, demonstrating glutamate regulation as a potential neuroprotective strategy in MS.
32
Wong, Laura Elisabeth, Molly E. Gibson, H. Moore Arnold, Blake Pepinsky, and Eric Frank. "Artemin promotes functional long-distance axonal regeneration to the brainstem after dorsal root crush." Proceedings of the National Academy of Sciences 112, no. 19 (April 27, 2015): 6170–75. http://dx.doi.org/10.1073/pnas.1502057112.
Full textAbstract:
Recovery after a spinal cord injury often requires that axons restore synaptic connectivity with denervated targets several centimeters from the site of injury. Here we report that systemic artemin (ARTN) treatment promotes the regeneration of sensory axons to the brainstem after brachial dorsal root crush in adult rats. ARTN not only stimulates robust regeneration of large, myelinated sensory axons to the brainstem, but also promotes functional reinnervation of the appropriate target region, the cuneate nucleus. ARTN signals primarily through the RET tyrosine kinase, an interaction that requires the nonsignaling coreceptor GDNF family receptor (GFRα3). Previous studies reported limited GFRα3 expression on large sensory neurons, but our findings demonstrate that ARTN promotes robust regeneration of large, myelinated sensory afferents. Using a cell sorting technique, we demonstrate that GFRα3 expression is similar in myelinated and unmyelinated adult sensory neurons, suggesting that ARTN likely induces long-distance regeneration by binding GFRα3 and RET. Although ARTN is delivered for just 2 wk, regeneration to the brainstem requires more than 3 mo, suggesting that brief trophic support may initiate intrinsic growth programs that remain active until targets are reached. Given its ability to promote targeted functional regeneration to the brainstem, ARTN may represent a promising therapy for restoring sensory function after spinal cord injury.
33
Szymanski, Linda J., Debra Hawes, and Floyd Gilles. "Corticospinal Wallerian Degeneration Before Myelination: A Case Report." Pediatric and Developmental Pathology 23, no. 5 (May 14, 2020): 399–403. http://dx.doi.org/10.1177/1093526620923452.
Full textAbstract:
Wallerian degeneration is defined as axonal fiber and myelin sheath degeneration that affects myelinated axons within the peripheral or central nervous system. Wallerian degeneration or anterograde axonal degeneration before myelination is rarely reported. Involvement of both corticospinal tracts (CSTs) is rarely documented in the literature. We present the postmortem neuropathologic findings of a 1-week-old male neonate born at 23 weeks of gestation with bilateral CST degeneration extending from the posterior limb of the internal capsule through the brainstem into the lumbar spinal cord. Abundant CD68- and CD163-positive macrophages were the prominent histopathology in both CSTs. The cerebrum, brainstem, and spinal cord were unmyelinated, as expected. In contrast, the spinal nerve roots demonstrated early myelination. This case illustrates that Wallerian degeneration occurs in unmyelinated axis cylinders.
34
Fan, Wei, John H. Schild, and Michael C. Andresen. "Graded and dynamic reflex summation of myelinated and unmyelinated rat aortic baroreceptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (September 1, 1999): R748—R756. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r748.
Full textAbstract:
Unmyelinated (C) and myelinated (A) baroreceptor (BR) axons are present in rat aortic depressor nerve (ADN). With graded ADN electrical activation and anodal conduction blockade, reflex responses in anesthetized rats were assessed as changes in mean arterial pressure (MAP) and heart rate (HR). We tested the hypothesis that C-type BR inputs are effective at low frequencies because they outnumber A-type. Anodal current ( I an) reversibly eliminated all MAP and HR responses to A-selective stimuli. High intensities activated all ADN axons (A+C) and decreased MAP at lower frequencies (<10 Hz) than were effective with A-selective stimulation. I anreduced only MAP responses to >10-Hz ADN stimulation. Burst patterns significantly augmented A- but not C-selective reflex responses despite identical numbers of shocks per second. A-selective stimuli failed to evoke significant bradycardia even at 200 Hz. Maximum intensity stimuli plus I an (C selective) evoked less bradycardia than without I an (A+C), indicating supra-additive summation unlike the occlusive summation for MAP responses. However, activation of reduced numbers of C-type BRs with all A-type BRs suggests a strong A to C interaction in reflex bradycardia responses. Surprisingly, I an block of A-type conduction eliminated all reflex bradycardia at such submaximal intensities despite C conduction and depressor responses. A- and C-type BRs act synergistically, and A-type activity is absolutely required in cardiac but not in depressor pathways. Thus greater numbers do not appear to account for C-type BR efficacy, and critical interactions between these two sensory subtypes appear to occur differentially across cardiac and systemic baroreflex effector pathways.
35
Felsten, Gary. "Propagation of Action Potentials: An Active Participation Exercise." Teaching of Psychology 25, no. 2 (April 1998): 109–11. http://dx.doi.org/10.1207/s15328023top2502_6.
Full textAbstract:
In this article, I describe an active participation exercise that demonstrates the propagation of action potentials along unmyelinated and myelinated axons. This activity helps students visualize processes involved in the generation and propagation of action potentials and demonstrates the advantages of myelination. Students may also use the exercise to review the ionic basis of neural signaling. Students in 2 courses perceived the exercise to be among the most helpful, interesting, and fun approaches to learning this material. Objective tests provided limited support for the efficacy of the exercise.
36
Fink, B. R., and A. M. Cairns. "DIFFERENTIAL RESISTANCE OF INDIVIDUAL UNMYELINATED AND MYELINATED AXONS TO GLUCOSE DEFICIENCY OR ANOXIA." Anesthesiology 69, no. 3A (September 1, 1988): A361. http://dx.doi.org/10.1097/00000542-198809010-00360.
Full text
37
Jessen, K. R., R. Mirsky, and L. Morgan. "Myelinated, but not unmyelinated axons, reversibly down-regulate N-CAM in Schwann cells." Journal of Neurocytology 16, no. 5 (October 1987): 681–88. http://dx.doi.org/10.1007/bf01637659.
Full text
38
Andresen, Michael C., Mackenzie E. Hofmann, and Jessica A. Fawley. "The unsilent majority–TRPV1 drives “spontaneous” transmission of unmyelinated primary afferents within cardiorespiratory NTS." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 12 (December 15, 2012): R1207—R1216. http://dx.doi.org/10.1152/ajpregu.00398.2012.
Full textAbstract:
Cranial primary afferent sensory neurons figure importantly in homeostatic control of visceral organ systems. Of the two broad classes of visceral afferents, the role of unmyelinated or C-type class remains poorly understood. This review contrasts key aspects of peripheral discharge properties of C-fiber afferents and their glutamate transmission mechanisms within the solitary tract nucleus (NTS). During normal prevailing conditions, most information arrives at the NTS through myelinated A-type nerves. However, most of visceral afferent axons (75–90%) in NTS are unmyelinated, C-type axons. Centrally, C-type solitary tract (ST) afferent terminals have presynaptic transient receptor potential vanilloid type 1 (TRPV1) receptors. Capsaicin activation of TRPV1 blocks phasic or synchronous release of glutamate but facilitates release of glutamate from a separate pool of vesicles. This TRPV1-operated pool of vesicles is active at normal temperatures and is responsible for actively driving a 10-fold higher release of glutamate at TRPV1 compared with TRPV1− terminals even in the absence of afferent action potentials. This novel TRPV1 mechanism is responsible for an additional asynchronous release of glutamate that is not present in myelinated terminals. The NTS is rich with presynaptic G protein-coupled receptors, and the implications of TRPV1-operated glutamate offer unique targets for signaling in C-type sensory afferent terminals from neuropeptides, inflammatory mediators, lipid metabolites, cytokines, and cannabinoids. From a homeostatic view, this combination could have broad implications for integration in chronic pathological disturbances in which the numeric dominance of C-type endings and TRPV1 would broadly disturb multisystem control mechanisms.
39
Orimo, S., T. Uchihara, T. Kanazawa, Y. Itoh, K. Wakabayashi, A. Kakita, and H. Takahashi. "Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease." Neuropathology and Applied Neurobiology 37, no. 7 (October 27, 2011): 791–802. http://dx.doi.org/10.1111/j.1365-2990.2011.01194.x.
Full text
40
Barjas Qaswal, Abdallah. "The Myelin Sheath Maintains the Spatiotemporal Fidelity of Action Potentials by Eliminating the Effect of Quantum Tunneling of Potassium Ions through the Closed Channels of the Neuronal Membrane." Quantum Reports 1, no. 2 (December 6, 2019): 287–94. http://dx.doi.org/10.3390/quantum1020026.
Full textAbstract:
The myelin sheath facilitates action potential conduction along the axons, however, the mechanism by which myelin maintains the spatiotemporal fidelity and limits the hyperexcitability among myelinated neurons requires further investigation. Therefore, in this study, the model of quantum tunneling of potassium ions through the closed channels is used to explore this function of myelin. According to the present calculations, when an unmyelinated neuron fires, there is a probability of 9.15 × 10 − 4 that it will induce an action potential in other unmyelinated neurons, and this probability varies according to the type of channels involved, the channels density in the axonal membrane, and the surface area available for tunneling. The myelin sheath forms a thick barrier that covers the potassium channels and prevents ions from tunneling through them to induce action potential. Hence, it confines the action potentials spatiotemporally and limits the hyperexcitability. On the other hand, lack of myelin, as in unmyelinated neurons or demyelinating diseases, exposes potassium channels to tunneling by potassium ions and induces the action potential. This approach gives different perspectives to look at the interaction between neurons and explains how quantum physics might play a role in the actions occurring in the nervous system.
41
Cheepudomwit, Therapoj, Emre Güzelsu, Chunhua Zhou, John W. Griffin, and Ahmet Höke. "Comparison of cytokine expression profile during Wallerian degeneration of myelinated and unmyelinated peripheral axons." Neuroscience Letters 430, no. 3 (January 2008): 230–35. http://dx.doi.org/10.1016/j.neulet.2007.11.003.
Full text
42
Carter, Deborah A., and S. J. W. Lisney. "The numbers of unmyelinated and myelinated axons in normal and regenerated rat saphenous nerves." Journal of the Neurological Sciences 80, no. 2-3 (September 1987): 163–71. http://dx.doi.org/10.1016/0022-510x(87)90152-3.
Full text
43
Tremblay, Jacques P., Claude Gravel, and Richard B. Hawkes. "A monoclonal antibody to β-tubulin distinguishes a subset of neurons and axons in the chick ciliary ganglion." Canadian Journal of Biochemistry and Cell Biology 63, no. 6 (June 1, 1985): 458–69. http://dx.doi.org/10.1139/o85-065.
Full textAbstract:
A monoclonal antibody, called mabPS2, has been produced by injecting mice with purified postsynaptic densities from adult rat brain. The antibody reacts with an epitope of β-tubulin which is not found on the α-tubulin subunit. In the chick ciliary ganglion mabPS2 reacts both with some large and some small neurons. mabPS2 also labels a subset of myelinated, as well as some unmyelinated axons. Higher magnification of longitudinal sections of axons shows that the reaction product is associated with microtubules. The nerve terminals on the ciliary neurons are also labelled and at higher magnification the label is seen to be distributed generally throughout the cytosol and especially concentrated on the membranes of synaptic vesicles. mabPS2 can therefore be used a a differentiation marker for neurons in chick ciliary ganglion.
44
Silva-Alves, Kerly Shamyra, Francisco Walber Ferreira-da-Silva, Andrelina Noronha Coelho-de-Souza, and José Henrique Leal-Cardoso. "Essential Oil of Croton zehntneri Prevents Conduction Alterations Produced by Diabetes Mellitus on Vagus Nerve." Plants 10, no. 5 (April 28, 2021): 893. http://dx.doi.org/10.3390/plants10050893.
Full textAbstract:
Autonomic diabetic neuropathy (ADN) is a complication of diabetes mellitus (DM), to which there is no specific treatment. In this study, the efficacy of the essential oil of Croton zehntneri (EOCz) in preventing ADN was evaluated in the rat vagus nerve. For the two fastest conducting myelinated types of axons of the vagus nerve, the conduction velocities and rheobase decreased, whilst the duration of the components of the compound action potential of these fibers increased. EOCz completely prevented these DM-induced alterations of the vagus nerve. Unmyelinated fibers were not affected. In conclusion, this investigation demonstrated that EOCz is a potential therapeutic agent for the treatment of ADN.
45
Murakami, Mineko, Chizuka Ide, and Haruyuki Kanaya. "Regeneration in the rat optic nerve after cold injury." Journal of Neurosurgery 71, no. 2 (August 1989): 254–65. http://dx.doi.org/10.3171/jns.1989.71.2.0254.
Full textAbstract:
✓ In order to examine nerve regeneration under conditions in which the basal laminae of the glial limiting membranes (GLM) and blood vessels were preserved intact, the intraorbital segment of adult rat optic nerve was frozen locally. During the next 3 months, degenerative and regenerative changes in axons and glial cells were observed by light and electron microscopy. On the day after treatment, all the myelinated and unmyelinated axons in the central zone of the lesion were damaged. The astrocyte endfeet of the GLM as well as the blood vessels were extensively disrupted, while their basal laminae were preserved apparently intact as a continuous sheet. Three days after treatment, regenerating axons appeared in the central zone of the lesion. They contained various numbers of clear and dense-cored vesicles as well as some smooth endoplasmic reticulum. The regenerating axons gradually increased in number, especially beneath the pial and perivascular surfaces of the lesion, where an abundance of regenerating axons was found 3 months after treatment. A few of these axons were abnormally remyelinated by oligodendrocytes. In addition to this axonal regeneration through the intraoptic nerve compartment, fine regenerating axons were seen growing out through GLM into the pial connective tissue 3 weeks after treatment. Astrocyte endfeet of the GLM became irregular in contour, protruding in a fern-leaf fashion into the pial connective tissue. Fine naked axons grew out through these protrusions and subsequently increased in number, vigorously growing in large bundles both proximally and distally along blood vessels in the pial connective tissue. Bundles of regenerating axons extended as much as 1.5 mm from the site of the lesion 3 months after surgery. These bundles were covered by thin processes of pial or arachnoidal non-neuronal cells, and the regenerating axons remained unmyelinated. The above findings indicate that under well-nourished conditions, adult mammalian optic nerve exhibits considerable regenerative ability.
46
Campbell, Graham R., and Don J. Mahad. "Mitochondria as Crucial Players in Demyelinated Axons: Lessons from Neuropathology and Experimental Demyelination." Autoimmune Diseases 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/262847.
Full textAbstract:
Mitochondria are the most efficient producers of energy in the form of ATP. Energy demands of axons, placed at relatively great distances from the neuronal cell body, are met by mitochondria, which when functionally compromised, produce reactive oxygen species (ROS) in excess. Axons are made metabolically efficient by myelination, which enables saltatory conduction. The importance of mitochondria for maintaining the structural integrity of myelinated axons is illustrated by neuroaxonal degeneration in primary mitochondrial disorders. When demyelinated, the compartmentalisation of ion channels along axons is disrupted. The redistribution of electrogenic machinery is thought to increase the energy demand of demyelinated axons. We review related studies that focus on mitochondria within unmyelinated, demyelinated and dysmyelinated axons in the central nervous system. Based on neuropathological observations we propose the increase in mitochondrial presence within demyelinated axons as an adaptive process to the increased energy need. An increased presence of mitochondria would also increase the capacity to produce deleterious agents such as ROS when functionally compromised. Given the lack of direct evidence of a beneficial or harmful effect of mitochondrial changes, the precise role of increased mitochondrial presence within axons due to demyelination needs to be further explored in experimental demyelinationin-vivoandin-vitro.
47
Dietz, F. B., and R. A. Jaffe. "Bupivacaine-induced Differential Nerve Blockade in Single Myelinated and Unmyelinated Dorsal and Ventral Root Axons." Anesthesiology 81, SUPPLEMENT (September 1994): A1011. http://dx.doi.org/10.1097/00000542-199409001-01010.
Full text
48
Blenk, K. H., M. Michaelis, C. Vogel, and W. Janig. "Thermosensitivity of acutely axotomized sensory nerve fibers." Journal of Neurophysiology 76, no. 2 (August 1, 1996): 743–52. http://dx.doi.org/10.1152/jn.1996.76.2.743.
Full textAbstract:
1. Thermosensitivity of axotomized myelinated and unmyelinated fibers in the sural nerve was examined in anesthetized rats within 24 h after nerve ligation and transection. Activity in single fibers was recorded extracellularly from small filaments dissected from the nerve approximately 20-30 mm proximal to the lesioned site. Cold and warm stimuli were applied to the ligated and cut nerve end or 5-10 mm further proximal. 2. Among 871 unmyelinated fibers tested, 40 were excited by cooling of the cut and ligated nerve end (8-15 degrees C), 44 were excited by warming (35-65 degrees C), and 16 were both cold and warm sensitive. None of the 438 myelinated fibers investigated were activated by either cold or warm stimuli. 3. Cold- and warm-sensitive fibers responded in a graded fashion to thermal stimuli of variable temperatures. Between 11 and 30 degrees C, the responses of cold-sensitive fibers increased when the temperature was reduced. Responses of warm-sensitive fibers increased between 40 and 65 degrees C, when the temperature was increased. 4. Thermosensitive fibers displayed characteristic response profiles. Responses to cold stimuli were maximal at the beginning and decreased continuously to lower discharge frequencies as the stimuli were maintained. The stimulus-response curves to warm stimuli were bell-shaped and discharge frequencies were maximal after 5-15 s. 5. In some cold-sensitive fibers a spatial gradient of excitability emerged after axotomy. Maximal responses to isothermal stimuli were observed at the transection site, whereas the excitability declined when the thermal stimuli were applied 5 and 10 mm further proximal. 6. After axotomy, 190 unmyelinated fibers were exposed to cold and warm stimuli at two sites 5 and 10 mm proximal of the nerve stump, and 172 intact C fibers were stimulated at anatomically comparable sites along the nerve. No statistically significant difference was found between the prevalences of thermosensitivity of C fibers along their axons in these two groups (7 of 172 vs. 11 of 190). 7. In conclusion, some unmyelinated fibers can be ectopically excited by thermal stimuli within 24 h after nerve cut and ligation. This ectopically evoked activity may contribute to the generation of paresthesias, painful sensations, and associated changes following peripheral nerve lesion.
49
Braund, K. G., M. Toivio-Kinnucan, J. M. Vallat, J. R. Mehta, and D. C. Levesque. "Distal Sensorimotor Polyneuropathy in Mature Rottweiler Dogs." Veterinary Pathology 31, no. 3 (May 1994): 316–26. http://dx.doi.org/10.1177/030098589403100304.
Full textAbstract:
A polyneuropathy recognized in mature Rottweiler dogs is characterized by paraparesis that progresses to tetraparesis, spinal hyporeflexia and hypotonia, and appendicular muscle atrophy. Although signs may appear acutely, the course tends to be gradually progressive (up to 12 months or longer in some dogs) and may be relapsing. Nerve and muscle biopsies were examined from eight affected Rottweilers (six male and two female) between ages 1.5 and 4 years. Pronounced neurogenic atrophy was present in skeletal muscle samples. Changes in sensory and motor peripheral nerves included loss of myelinated nerve fibers, axonal necrosis, and variable numbers of fibers with inappropriately thin myelin sheaths. Ultrastructural findings included myelinated fibers showing myelinoaxonal necrosis, demyelinated fibers often associated with macrophage infiltration, many axons with myelinlike membranous profiles, increased endoneurial collagen, occasional axonal atrophy, and numerous Büngner bands. Lesions in unmyelinated fibers included increased numbers of Schwann cell profiles and loss of axons in Schwann cell subunits. Morphologic and morphometric studies indicated preferential loss of medium (5.5–8 μm) and large (8.5–12.5 μm) fibers, which was more severe in distal parts of nerves than in more proximal regions and nerve roots. The cause was not determined; however, histopathologic studies suggest this condition is a dying-back distal sensorimotor polyneuropathy that has morphologic and morphometric similarities to hereditary motor and sensory neuropathy (HMSN) type II in humans.
50
Coggeshall, Richard E., and Susan M. Carlton. "Ultrastructural analysis of NMDA, AMPA, and kainate receptors on unmyelinated and myelinated axons in the periphery." Journal of Comparative Neurology 391, no. 1 (December 6, 1998): 78–86. http://dx.doi.org/10.1002/(sici)1096-9861(19980202)391:1<78::aid-cne7>3.0.co;2-o.
Full text