Journal articles on the topic 'Axon reflex response'
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Lisney, SJW, and LAM Bharali. "The Axon Reflex: An Outdated Idea or a Valid Hypothesis?" Physiology 4, no. 2 (April 1, 1989): 45–48. http://dx.doi.org/10.1152/physiologyonline.1989.4.2.45.
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Physiology textbooks almost always include the axon reflex in the context of the triple response, often followed by the caveat that the evidence is either indirect or incomplete. Experimental work and ideas on the topic are reviewed, asking whether there now is a stronger case for axon reflex mechanisms.
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Shaw, Brian K., and William B. Kristan. "Relative Roles of the S Cell Network and Parallel Interneuronal Pathways in the Whole-Body Shortening Reflex of the Medicinal Leech." Journal of Neurophysiology 82, no. 3 (September 1, 1999): 1114–23. http://dx.doi.org/10.1152/jn.1999.82.3.1114.
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The whole-body shortening reflex of the medicinal leech Hirudo medicinalis is a withdrawal response produced by anterior mechanical stimuli. The interneuronal pathways underlying this reflex consist of the S cell network (a chain of electrically coupled interneurons) and a set of other, parallel pathways. We used a variety of techniques to characterize these interneuronal pathways further, including intracellular stimulation of the S cell network, photoablation of the S cell axon, and selective lesions of particular connectives (the axon bundles that link adjacent ganglia in the leech nerve cord). These experiments demonstrated that the S cell network is neither sufficient nor necessary for the production of the shortening reflex. The axons of the parallel pathways were localized to the lateral connectives (whereas the S cell axon runs through the medial connective). We used physiological techniques to show that the axons of the parallel pathways have a larger diameter in the anterior connective and to demonstrate that the parallel pathways are activated selectively by anterior mechanosensory stimuli. We also presented correlative evidence that the parallel pathways, along with activating motor neurons during shortening, are responsible for inhibiting a higher-order “command-like” interneuron in the neuronal circuit for swimming, thus playing a role in the behavioral choice between swimming and shortening.
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Montserrat, Luis, and Manuel Benito. "Motor reflex responses elicited by cutaneous stimulation in the regenerating nerve of man: Axon reflex or ephaptic response?" Muscle & Nerve 13, no. 6 (June 1990): 501–7. http://dx.doi.org/10.1002/mus.880130606.
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Minson, Christopher T., Latoya T. Berry, and Michael J. Joyner. "Nitric oxide and neurally mediated regulation of skin blood flow during local heating." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1619–26. http://dx.doi.org/10.1152/jappl.2001.91.4.1619.
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The mechanisms underlying the skin blood flow (SkBF) response to local heating are complex and poorly understood. Our goal was to examine the role of axon reflexes and nitric oxide (NO) in the SkBF response to a local heating protocol. We performed 40 experiments following a standardized heating protocol with different interventions, including blockade of the axon reflex (EMLA cream), antebrachial nerve blockade (0.5% bupivacaine injection), and NO synthase (NOS) inhibition (≥10 mM N G-nitro-l-arginine methyl ester; microdialysis). Appropriate controls were performed to verify the efficacy of the various blocks. Values are expressed as a percentage of maximal SkBF (SkBFmax; 50 mM sodium nitroprusside). At the initiation of local heating, SkBF rose to an initial peak, followed by a brief nadir, and a secondary, progressive rise to a plateau. Axon reflex block decreased the initial peak from 75+3 to 32 ± 2% SkBFmax ( P< 0.01 vs. control) but did not affect the plateau. NOS inhibition before and throughout local heating reduced the initial peak from 75 ± 3 to 56 ± 3% SkBFmax ( P< 0.01) and the plateau from 87 ± 4 to 40 ± 5%. NOS inhibition during axon reflex block did not further reduce the initial SkBF peak compared with axon reflex block alone. Antebrachial nerve block did not affect the local heating SkBF response. The primary finding of these studies is that there are at least two independent mechanisms contributing to the rise in SkBF during nonpainful local heating: a fast-responding vasodilator system mediated by the axon reflexes and a more slowly responding vasodilator system that relies on local production of NO.
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Kimura, Kenichi, Hayato Takeuchi, Kuniko Yuri, and Ikuro Wakayama. "Effects of Nitric Oxide Synthase Inhibition on Cutaneous Vasodilation in Response to Acupuncture Stimulation in Humans." Acupuncture in Medicine 31, no. 1 (March 2013): 74–80. http://dx.doi.org/10.1136/acupmed-2012-010177.
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Objectives The aim of the present study was to elucidate the mechanism of cutaneous vasodilation following acupuncture stimulation by investigating the roles of nitric oxide (NO) and axon reflex vasodilation. Methods The subjects were 17 healthy male volunteers. The role of NO was investigated by administering NG-nitro-L-arginine methyl ester hydrochloride (L-NAME, 20 mM), an NO synthase inhibitor or Ringer's solution (control site), via intradermal microdialysis (protocol 1; n=7). The role of axon reflex vasodilation by local sensory neurones was investigated by comparing vasodilation at sites treated with ‘eutectic mixture of local anaesthetics’ (EMLA) cream (2.5% lidocaine and 2.5% prilocaine) with untreated sites (control site) (protocol 2; n=10). After 5 min of baseline recording, acupuncture was applied to PC4 and a control site in proximity to PC4 for 10 min and scanning was performed for 60 min after acupuncture stimulation. Skin blood flow (SkBF) was evaluated by laser Doppler perfusion imaging. Cutaneous vascular conductance (CVC) was calculated from the ratio of SkBF to mean arterial blood pressure. Results In the first protocol, sites administered L-NAME showed significant reductions in CVC responses following acupuncture stimulation compared to control sites (administered Ringer's solution) (p<0.05). In the second protocol, changes in CVC responses after acupuncture stimulation did not differ significantly between treated sites with EMLA cream and untreated sites (p>0.05). Conclusions These data suggest that cutaneous vasodilation in response to acupuncture stimulation may not occur through an axon reflex as previously reported. Rather, NO mechanisms appear to contribute to the vasodilator response.
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Minson, Christopher T., Lacy A. Holowatz, Brett J. Wong, W. Larry Kenney, and Brad W. Wilkins. "Decreased nitric oxide- and axon reflex-mediated cutaneous vasodilation with age during local heating." Journal of Applied Physiology 93, no. 5 (November 1, 2002): 1644–49. http://dx.doi.org/10.1152/japplphysiol.00229.2002.
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Cutaneous vasodilation is reduced in healthy older vs. young subjects; however, the mechanisms that underlie these age-related changes are unclear. Our goal in the present study was to determine the role of nitric oxide (NO) and the axon reflexes in the skin blood flow (SkBF) response to local heating with advanced age. We placed two microdialysis fibers in the forearm skin of 10 young (Y; 22 ± 2 yr) and 10 older (O; 77 ± 5 yr) men and women. SkBF over each site was measured by laser-Doppler flowmetry (LDF; Moor DRT4). Both sites were heated to 42°C for ∼60 min while 10 mM N G-nitro-l-arginine methyl ester (l-NAME) was infused throughout the protocol to inhibit NO synthase (NOS) in one site and 10 mM l-NAME was infused after 40 min of local heating in the second site. Data were expressed as a percentage of maximal vasodilation (%CVCmax; 28 mM nitroprusside infusion). Local heating beforel-NAME infusion resulted in a significantly reduced initial peak (Y: 61 ± 2%CVCmax vs. O: 46 ± 4%CVCmax) and plateau (Y: 93 ± 2%CVCmaxvs. O: 82 ± 5%CVCmax) CVC values in older subjects ( P < 0.05). When NOS was inhibited after 40 min of heating, CVC declined to the same value in the young and older groups. Thus the overall contribution of NO to the plateau phase of the SkBF response to local heating was less in the older subjects. The initial peak response was significantly lower in the older subjects in both microdialysis sites (Y: 52 ± 4%CVCmax vs. O: 38 ± 5%CVCmax; P < 0.05). These data suggest that age-related changes in both axon reflex-mediated and NO-mediated vasodilation contribute to attenuated cutaneous vasodilator responses in the elderly.
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Maselli, Ricardo A., Jonathan B. Jaspan, Betty C. Soliven, Andrew J. Green, Jean-Paul Spire, and Barry G. W. Arnason. "Comparison of sympathetic skin response with quantitative sudomotor axon reflex test in diabetic neuropathy." Muscle & Nerve 12, no. 5 (May 1989): 420–23. http://dx.doi.org/10.1002/mus.880120513.
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Terkelsen, Astrid J., Janne Gierthmühlen, Nanna B. Finnerup, Anders P. Højlund, and Troels S. Jensen. "Bilateral Hypersensitivity to Capsaicin, Thermal, and Mechanical Stimuli in Unilateral Complex Regional Pain Syndrome." Anesthesiology 120, no. 5 (May 1, 2014): 1225–36. http://dx.doi.org/10.1097/aln.0000000000000220.
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Abstract Background: Complex regional pain syndrome is multifactorial. Exaggerated inflammatory responses to limb injury may be involved. The authors hypothesized that capsaicin-induced pain and neurogenic inflammation (skin perfusion and flare area) are increased in patients with complex regional pain syndrome compared with that in controls. Methods: Twenty patients with unilateral upper-limb complex regional pain syndrome and 20 age-, sex-, and body mass index–matched controls participated. Topical capsaicin 5% was applied to the back of both hands for 30 min, and pain intensity was assessed on a visual analogue scale. A laser Doppler perfusion imager scanner estimated capsaicin-induced skin perfusion and flare area. Autonomic and small-fiber function was assessed by sensory testing, quantitative sudomotor axon reflex test, and vasoconstrictor responses. Results: The authors found bilateral hypersensitivity to capsaicin (P ≤ 0.02), skin fold (P = 0.001), joint pressure (P < 0.0001), cold (P ≤ 0.01), and heat pain (P ≤ 0.04) in patients compared with that in controls and thermal and mechanical hyperalgesia in the complex regional pain syndrome–affected hand compared with that in the unaffected hand (P ≤ 0.001). The patients had normal capsaicin-induced flare areas, thermal detection thresholds, quantitative sudomotor axon reflex test, and vasoconstrictor responses. Conclusions: The main finding is bilaterally increased capsaicin-induced pain in patients compared with controls. The flare response to capsaicin was normal, suggesting that the increased pain response was not due to increased neurogenic inflammation. The bilateral hypersensitivity to painful chemical, thermal, and mechanical stimuli not confined to the innervation area of a peripheral nerve or root cannot be explained by a regional change and may partly be due to central sensitization.
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Millet, Claire, Matthieu Roustit, Sophie Blaise, and Jean-Luc Cracowski. "Aging is associated with a diminished axon reflex response to local heating on the gaiter skin area." Microvascular Research 84, no. 3 (November 2012): 356–61. http://dx.doi.org/10.1016/j.mvr.2012.06.009.
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Plinta, Aelita, Pēteris Tretjakovs, Ināra Logina, Indra Miķelsone, Leons Blumfelds, and Guntis Bahs. "Influence of Migraine on Axon Reflex-Mediated and Endothelial-Dependent Vasodilatation in the Skin." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 75, no. 3 (June 1, 2021): 194–99. http://dx.doi.org/10.2478/prolas-2021-0023.
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Abstract The aim of the study was to evaluate the changes in skin blood flow as a result of local heating tests in migraine patients during the interictal period, measured by laser Doppler perfusion imaging (LDI). The aim of the study was also to estimate the correlations between the results of these tests and interleukin (IL)-8 levels. Twelve migraine patients during their interictal period were compared with twelve healthy control subjects. Only women were included in the study. Both groups were matched with regard of their age, body mass index and blood pressure. For the purpose of measuring cutaneous microvascular blood flow, heating (+44 °C) of the dorsal side of the palm as a response to the local LDI was used. IL-8 was measured in serum by ELISA method. The findings suggested that migraine patients have a cutaneous vasomotor dysfunction during the interictal period. The results showed a significant decrease in the initial peak of vasodilation and the second peak of vasodilation (plateau phase). Also there were significant changes observed in the length of the time interval required to reach the first and second vasodilation peak. It is known that migraine patients have a shorter time interval to reach the first perfusion peak (axonal reflex-mediated) and longer time interval to reach the second peak (endothelium-dependent). The results confirmed the correlation between proinflammatory chemokine IL-8 levels, and the time interval till the second peak of blood flow in all study subjects.
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Tartas, Maylis, Philippe Bouyé, Audrey Koïtka, Sylvain Durand, Yves Gallois, Jean Louis Saumet, and Pierre Abraham. "Early vasodilator response to anodal current application in human is not impaired by cyclooxygenase-2 blockade." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 4 (April 2005): H1668—H1673. http://dx.doi.org/10.1152/ajpheart.00415.2004.
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It is generally acknowledged that cutaneous vasodilatation in response to monopolar galvanic current application would result from an axon reflex in primary afferent fibers and the neurogenic inflammation resulting from neuropeptide release. Previous studies suggested participation of prostaglandin (PG) in anodal current-induced cutaneous vasodilatation. Thus the inducible cyclooxygenase (COX) isoform (COX-2), assumed to play a key role in inflammation, should be involved in the synthesis of the PG that is released. Skin blood flow (SkBF) variations induced by 5 min of 0.1-mA monopolar anodal current application were evaluated with laser-Doppler flowmetry on the forearm of healthy volunteers treated with indomethacin (COX-1 and COX-2 inhibitor), celecoxib (COX-2 inhibitor), or placebo. SkBF was indexed as cutaneous vascular conductance (CVC), expressed as percentage of heat-induced maximal CVC (%MVC). Urinalyses were performed to test celecoxib treatment efficiency. No difference was found in CVC values at rest: 14.3 ± 4.0, 11.9 ± 3.2, and 10.9 ± 2.0% MVC after indomethacin, celecoxib, and placebo treatment, respectively. At 10 min after the onset of anodal current application, CVC values were 22.2 ± 4.9% MVC (not significantly different from rest) with indomethacin, 85.7 ± 15.3% MVC ( P < 0.001 vs. rest) with celecoxib, and 70.4 ± 13.1% MVC ( P < 0.001 vs. rest) with placebo. Celecoxib significantly depressed the urinary prostacyclin metabolite 6-keto-PGF1α ( P < 0.05 vs. placebo). Indomethacin, but not celecoxib, significantly inhibited the anodal current-induced vasodilatation. Thus, although they are assumed to result from an axon reflex in primary afferent fibers and neurogenic inflammation, these results suggest that the early anodal current-induced vasodilatation is mainly dependent on COX-1-induced PG synthesis.
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Medow, Marvin S., Arun Aggarwal, Ila Baugham, Zachary Messer, and Julian M. Stewart. "Modulation of the axon-reflex response to local heat by reactive oxygen species in subjects with chronic fatigue syndrome." Journal of Applied Physiology 114, no. 1 (January 1, 2013): 45–51. http://dx.doi.org/10.1152/japplphysiol.00821.2012.
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Local cutaneous heating causes vasodilation as an initial first peak, a nadir, and increase to plateau. Reactive oxygen species (ROS) modulate the heat plateau in healthy controls. The initial peak, due to C-fiber nociceptor-mediated axon reflexes, is blunted with local anesthetics and may serve as a surrogate for the cutaneous response to peripheral heat. Chronic fatigue syndrome (CFS) subjects report increased perception of pain. To determine the role of ROS in this neurally mediated response, we evaluated changes in cutaneous blood flow from local heat in nine CFS subjects (16–22 yr) compared with eight healthy controls (18–26 yr). We heated skin to 42°C and measured local blood flow as a percentage of maximum cutaneous vascular conductance (%CVCmax). Although CFS subjects had significantly lower baseline flow [8.75 ± 0.56 vs. 12.27 ± 1.07 (%CVCmax, CFS vs. control)], there were no differences between groups to local heat. We then remeasured this with apocynin to inhibit NADPH oxidase, allopurinol to inhibit xanthine oxidase, tempol to inhibit superoxide, and ebselen to reduce H2O2. Apocynin significantly increased baseline blood flow (before heat, 14.91 ± 2.21 vs. 8.75 ± 1.66) and the first heat peak (69.33 ± 3.36 vs. 59.75 ± 2.75). Allopurinol and ebselen only enhanced the first heat peaks (71.55 ± 2.48 vs. 61.72 ± 2.01 and 76.55 ± 5.21 vs. 58.56 ± 3.66, respectively). Tempol had no effect on local heating. None of these agents changed the response to local heat in control subjects. Thus the response to heat may be altered by local levels of ROS, particularly H2O2 in CFS subjects, and may be related to their hyperesthesia/hyperalgesia.
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Ives, Colleen T., Michael J. Berger, and Kurt Kimpinski. "The Autonomic Reflex Screen in Healthy Participants from Southwestern Ontario." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 40, no. 6 (November 2013): 848–53. http://dx.doi.org/10.1017/s0317167100016000.
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Background:The autonomic reflex screen (ARS) is a composite of well-defined tests of various autonomic domains and is an essential part of the diagnosis of autonomic disorders. Institutional and regional differences exist and necessitate the ongoing development of control values for the ARS. Here we present data obtained from healthy participants from Southwestern Ontario.Methods:A total of 121 healthy individuals underwent quantitative sudomotor axon reflex testing (QSART), heart rate response to deep breathing (HRDB), and Valsalva maneuver using standard protocols as part of the ARS.Results:Sweat volumes obtained during QSART are presented by site (forearm, proximal leg, distal leg and foot) and by gender. Data is expressed as the mean sweat volume per site with the associated 2.5th, 5th and 95th percentiles. Data for males and females is also stratified by age group (14-25, 26-40 and 41-76 years). Measurements of cardiovagal parasympathetic function including HRDB and Valsalva ratio are stratified by age group (14-25, 26- 40 and 41-76 years). Data is expressed as the mean with associated percentiles (2.5, 5, 95 and 97.5 percentiles).Conclusions:The current manuscript provides control data for the various components of the ARS to aid in the diagnosis of autonomic disorders.
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Metzler-Wilson, Kristen, Thad E. Wilson, Samantha M. Ausmus, and Austin M. Sventeckis. "Effect of sensory blockade and rate of sensory stimulation on local heating induced axon reflex response in facial skin." Autonomic Neuroscience 233 (July 2021): 102809. http://dx.doi.org/10.1016/j.autneu.2021.102809.
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Gokin, A. P., L. J. Jennings, and G. M. Mawe. "Actions of calcitonin gene-related peptide in guinea pig gallbladder ganglia." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 5 (November 1, 1996): G876—G883. http://dx.doi.org/10.1152/ajpgi.1996.271.5.g876.
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The actions of calcitonin gene-related peptide (CGRP) have been determined from intracellular recordings obtained from gallbladder neurons in intact whole mount preparations. In most cells, pressure microejection of CGRP elicited a slow, monophasic depolarization, 4 mV in amplitude, that was associated with a decrease in input resistance and increased excitability. The CGRP-induced depolarization was attenuated in a low-Na+ solution and had a reversal potential of -8 mV. In 10% of the cells, microejection of CGRP elicited a biphasic response that was composed of a rapid transient depolarization followed by a slow depolarization that was similar to the monophasic response. Addition of CGRP (1–10 nM) to the bathing solution elicited a monophasic depolarization and desensitized the cells to applications of CGRP by microejection. Forskolin, applied either by microejection or bath application, also depolarized gallbladder neurons and produced cross-desensitization to CGRP. Responses to substance P were not enhanced by CGRP, and CGRP did not affect fast synaptic responses. It is concluded that CGRP may contribute to a local axon reflex response in gallbladder ganglia.
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Siepmann, Timo, Elka Frenz, Ana Isabel Penzlin, Susan Goelz, Wagner Zago, Ingeborg Friehs, Marie Luise Kubasch, et al. "Pilomotor function is impaired in patients with Parkinson's disease: A study of the adrenergic axon-reflex response and autonomic functions." Parkinsonism & Related Disorders 31 (October 2016): 129–34. http://dx.doi.org/10.1016/j.parkreldis.2016.08.001.
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Mackie, G. O. "Giant axons and control of jetting in the squid Loligo and the jellyfish Aglantha." Canadian Journal of Zoology 68, no. 4 (April 1, 1990): 799–805. http://dx.doi.org/10.1139/z90-115.
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Both Loligo and Aglantha have sets of giant axons arranged in a cascading series, which transmit impulses at high velocity and with short synaptic delays to the swimming muscles. The layout of the axons is such as to guarantee symmetrical, near-simultaneous contractions of all parts of the swimming muscles, necessary for effective jetting. The giant axons in both animals are multinucleate, syncytial structures. In both animals, the first-order giants receive a rich afferent innervation. Despite these similarities in the layout and properties of their giant axon systems, Loligo and Aglantha control their swimming muscles in very different ways. The most striking difference is that Loligo has separate fast and slow innervations as well as fast and slow muscles, whereas Aglantha has only one innervation and one set of muscles, but can produce two types of contraction by switching between rapidly propagated sodium spikes and slowly propagated calcium spikes in its giant motor axons. A second major difference emerging from recent investigations is that whereas Aglantha uses its fast impulse propagation system for a conventional, short-latency escape response, squid appear (at least in laboratory studies) to use their fast pathway merely to augment the power of contractions brought about by their slow innervation, making no use of the potential the giant fibres hold for short-latency, reflex escape behaviour.
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Houghton, Belinda L., Jessica R. Meendering, Brett J. Wong, and Christopher T. Minson. "Nitric oxide and noradrenaline contribute to the temperature threshold of the axon reflex response to gradual local heating in human skin." Journal of Physiology 572, no. 3 (April 21, 2006): 811–20. http://dx.doi.org/10.1113/jphysiol.2005.104067.
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Cooke, H. J., M. Sidhu, P. Fox, Y. Z. Wang, and E. M. Zimmermann. "Substance P as a mediator of colonic secretory reflexes." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 2 (February 1, 1997): G238—G245. http://dx.doi.org/10.1152/ajpgi.1997.272.2.g238.
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The role of substance P in neural reflex pathways activated by stroking was investigated in muscle-stripped segments of distal colon from guinea pigs. Stroking the mucosal surface with a brush at 1 stroke/s evoked an increase in short-circuit current (Isc) indicative of chloride secretion. The response to mucosal stroking was maximally reduced by 69-75% by the antagonist GR-82334. The agonist [Sar9,Met(O2)11] substance P caused a bumetanide-sensitive increase in Isc when added to the mucosal or serosal bath. Ablation of extrinsic afferents with acute or chronic administration of capsaicin did not alter the mucosal stroking response. Reverse transcription-polymerase chain reaction and in situ hybridization revealed the presence of neurokinin1 (NK1) receptor messenger RNA in isolated colonocytes or crypt glands. Ligand binding of 125I-Bolton-Hunter-labeled substance P was inhibited by GR-82334. The 50% inhibitory concentration was 0.84 nM. The results demonstrate a role for substance P released from capsaicin-insensitive submucosal neurons and in mucosal stroking reflexes. The presence of NK1 receptors on isolated colonocytes suggests that appropriate elements are present for axon reflex activation of intestinal epithelial cells.
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Andersen, Erling Bo, Finn Boesen, Ole Henriksen, and Michael Sonne. "Blood flow in skeletal muscle of tetraplegic man during postural changes." Clinical Science 70, no. 4 (April 1, 1986): 321–25. http://dx.doi.org/10.1042/cs0700321.
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1. Relative changes in blood flow and vascular resistance in arm and leg muscle during head-up tilt at 45° were studied in eight patients with complete cervical spinal cord transection and in 13 healthy volunteers. 2. Muscle blood flow was measured by the local 133Xe washout method. 3. In forearm muscle kept at heart level blood flow remained constant in the tetraplegic patients during head-up tilt, in contrast to that seen in the normal subjects, where blood flow decreased by 30%. In the dependent leg muscle, head-up tilt caused a decrease in blood flow of 46% and 40% in the patients and normals, respectively. Abolition of the local veno-arteriolar axon reflex, by inducing local counter-pressure to prevent venous distension in the dependent leg muscle, reduced the decrease in blood flow to 24% and 23%, respectively. Thus, the vascular response to head-up tilt differed significantly in forearm muscle between the two groups, whereas no difference was seen in the leg muscle. 4. The absence of the vasoconstrictor response in forearm muscle indicates that postural sympathetic reflexes to this region depend on sympathetic reflexes integrated in centres located rostrally to the spinal cord. The results further suggest that local veno-arteriolar axon reflexes as well as spinal reflexes contribute to the observed vasoconstriction in the leg muscle.
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Aniss, A. M., H. C. Diener, J. Hore, D. Burke, and S. C. Gandevia. "Reflex activation of muscle spindles in human pretibial muscles during standing." Journal of Neurophysiology 64, no. 2 (August 1, 1990): 671–79. http://dx.doi.org/10.1152/jn.1990.64.2.671.
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1. Experiments were performed in standing subjects to determine whether low-threshold cutaneous and muscle afferents from mechanoreceptors in the human foot reflexly influence fusimotor neurons innervating pretibial flexor muscles. Recordings were made from 30 identified muscle-spindle afferents, four tendon-organ afferents, and one alpha-motor axon innervating the pretibial flexor muscles. The subjects stood without support or vision on a force platform while trains of electrical stimuli (5 stimuli, 300 Hz) were delivered at nonpainful intensities to the sural nerve or to the posterior tibial nerve at the ankle. 2. Seventeen of the 30 spindle endings had no background discharge, and none was activated by the sural or posterior tibial stimuli. Five silent afferents were given a background discharge by sustained pressure on the relevant tendon, but with two the discharge was dominated by a tremor rhythm obscuring any reflex response to the stimuli. Based on peristimulus time histograms (PSTHs), the sural stimuli then produced increases in discharge of two of the remaining three endings at latencies of 84 and 90 ms. These effects could not be explained by muscle stretch and are presumed to have been fusimotor mediated. 3. When the subjects stood freely without support or vision, 13 muscle-spindle endings had a background discharge, but with three endings tremor developed at the ankle and dominated the spindle discharge. Sural stimuli affected the discharge of five of nine endings unaffected by tremor. With three of these endings, there were changes in discharge that could be explained by muscle stretch.(ABSTRACT TRUNCATED AT 250 WORDS)
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Johnson, John M., and Dean L. Kellogg. "Local thermal control of the human cutaneous circulation." Journal of Applied Physiology 109, no. 4 (October 2010): 1229–38. http://dx.doi.org/10.1152/japplphysiol.00407.2010.
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The level of skin blood flow is subject to both reflex thermoregulatory control and influences from the direct effects of warming and cooling the skin. The effects of local changes in temperature are capable of maximally vasoconstricting or vasodilating the skin. They are brought about by a combination of mechanisms involving endothelial, adrenergic, and sensory systems. Local warming initiates a transient vasodilation through an axon reflex, succeeded by a plateau phase due largely to nitric oxide. Both phases are supported by sympathetic transmitters. The plateau phase is followed by the die-away phenomenon, a slow reversal of the vasodilation that is dependent on intact sympathetic vasoconstrictor nerves. The vasoconstriction with local skin cooling is brought about, in part, by a postsynaptic upregulation of α2c-adrenoceptors and, in part, by inhibition of the nitric oxide system at at least two points. There is also an early vasodilator response to local cooling, dependent on the rate of cooling. The mechanism for that transient vasodilation is not known, but it is inhibited by intact sympathetic vasoconstrictor nerve function and by intact sensory nerve function.
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Barman, S. M., and G. L. Gebber. "Axonal projection patterns of ventrolateral medullospinal sympathoexcitatory neurons." Journal of Neurophysiology 53, no. 6 (June 1, 1985): 1551–66. http://dx.doi.org/10.1152/jn.1985.53.6.1551.
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We studied the following properties of cat ventrolateral medullary (VLM) neurons that projected to the thoracic spinal cord: the relationship between their spontaneous activity and that in the inferior cardiac postganglionic sympathetic nerve, their responses to baroreceptor-reflex activation, their axonal conduction velocities, the funicular trajectories of their axons, the likely sites of termination of their axons, and their axonal branching patterns. Microstimulation in the second thoracic spinal segment (T2) antidromically activated 67 VLM neurons (as determined with time-controlled collision of spontaneous and evoked action potentials), whose activity was correlated to inferior cardiac sympathetic nerve discharge (as determined with spike-triggered averaging). We tested the effect of baroreceptor-reflex activation on the firing rate of 20 of these VLM-spinal neurons. Because the firing rate decreased in each instance, these neurons apparently subserved a sympathoexcitatory function. The axonal branching patterns of 51 VLM-spinal sympathoexcitatory neurons were studied. Thirty-four neurons were antidromically activated by stimulation in the T2 gray matter and in more caudal thoracic spinal segments (T11 and/or T6). In each case, the antidromic response evoked by stimulation in the T2 gray matter was due to activation of an axonal branch rather than the main axon (via current spread to the white matter). This was demonstrated with tests that included time-controlled collision of the action potentials initiated by stimulation in T2 and a more caudal thoracic spinal segment. Some VLM-spinal axons that projected to T11 branched in T6 as well as in T2. These data indicate that some VLM-spinal neurons exerted widespread excitatory influences on sympathetic outflow. Seventeen VLM sympathoexcitatory neurons that innervated the T2 gray matter could not be antidromically activated by stimulation in T5, T6, and T11 despite an extensive search at each level. Thus the axonal projections of some VLM-spinal neurons were restricted to upper thoracic segments. Antidromic mapping in T2 revealed that the axons of VLM sympathoexcitatory neurons coursed through the dorsolateral or ventrolateral funiculus to innervate the region of the intermediolateral nucleus. Mean axonal conduction velocity was 3.5 +/- 0.3 m/s. Those VLM-spinal axons restricted to upper thoracic segments generally were located dorsally and/or medially to those that innervated widely separated thoracic segments. The discharges of 35 other VLM neurons that were antidromically activated by T2 stimulation were not related to sympathetic nerve activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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Brandt, Jaclyn, Jonathan T. Evans, Taylor Mildenhall, Amanda Mulligan, Aimee Konieczny, Samuel J. Rose, and Arthur W. English. "Delaying the onset of treadmill exercise following peripheral nerve injury has different effects on axon regeneration and motoneuron synaptic plasticity." Journal of Neurophysiology 113, no. 7 (April 2015): 2390–99. http://dx.doi.org/10.1152/jn.00892.2014.
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Transection of a peripheral nerve results in withdrawal of synapses from motoneurons. Some of the withdrawn synapses are restored spontaneously, but those containing the vesicular glutamate transporter 1 (VGLUT1), and arising mainly from primary afferent neurons, are withdrawn permanently. If animals are exercised immediately after nerve injury, regeneration of the damaged axons is enhanced and no withdrawal of synapses from injured motoneurons can be detected. We investigated whether delaying the onset of exercise until after synapse withdrawal had occurred would yield similar results. In Lewis rats, the right sciatic nerve was cut and repaired. Reinnervation of the soleus muscle was monitored until a direct muscle (M) response was observed to stimulation of the tibial nerve. At that time, rats began 2 wk of daily treadmill exercise using an interval training protocol. Both M responses and electrically-evoked H reflexes were monitored weekly for an additional seven wk. Contacts made by structures containing VGLUT1 or glutamic acid decarboxylase (GAD67) with motoneurons were studied from confocal images of retrogradely labeled cells. Timing of full muscle reinnervation was similar in both delayed and immediately exercised rats. H reflex amplitude in delayed exercised rats was only half that found in immediately exercised animals. Unlike immediately exercised animals, motoneuron contacts containing VGLUT1 in delayed exercised rats were reduced significantly, relative to intact rats. The therapeutic window for application of exercise as a treatment to promote restoration of synaptic inputs onto motoneurons following peripheral nerve injury is different from that for promoting axon regeneration in the periphery.
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Safder, Shaista, Thomas C. Chelimsky, Mary Ann O'Riordan, and Gisela Chelimsky. "Autonomic Testing in Functional Gastrointestinal Disorders: Implications of Reproducible Gastrointestinal Complaints during Tilt Table Testing." Gastroenterology Research and Practice 2009 (2009): 1–6. http://dx.doi.org/10.1155/2009/868496.
Full textAbstract:
Background: The pathophysiology of functional abdominal pain (FAP) is unknown. The upright portion of a tilt table test triggers typical symptoms in certain children. Aim: To compare the pathophysiology and treatment response of children with FAP whose gastrointestinal symptoms (GI) were replicated (RGI) by tilt table testing (TTT) to those in whom TTT did not have this effect (NRGI).Methods: An IRB-approved retrospective review of the autonomic laboratory database identified all children tested for GI complaints. We compared results of TTT, Valsalva maneuver, deep breathing and the axon reflex sweat test. Overall treatment response and that specific to fludrocortisone was ranked from 1 to 5, with 1 “much worse,” 3 “neutral,” and 5 “much better.”Results: 32/76 identified children had reproducible symptoms on TTT (RGI) and 44 did not (NRGI). The RGI group was younger, had a shorter duration of symptoms, more postural tachycardia syndrome (POTS) and benefited more from fludrocortisone (73% in RGI vs. 25% in NRGI).Conclusion: Dividing patients with FAP according to the effect of TTT on their symptoms appears to delineate 2 fundamentally different groups, with potentially different pathophysiologies and treatment responses. A prospective study is needed.
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Cheshire, William P. "Sudomotor Dysfunction." Seminars in Neurology 40, no. 05 (September 9, 2020): 560–68. http://dx.doi.org/10.1055/s-0040-1713847.
Full textAbstract:
AbstractDisorders of sudomotor function are common and diverse in their presentations. Hyperhidrosis or hypohidrosis in generalized or regional neuroanatomical patterns can provide clues to neurologic localization and inform neurologic diagnosis. Conditions that impair sudomotor function include small fiber peripheral neuropathy, sudomotor neuropathy, myelopathy, α-synucleinopathies, autoimmune autonomic ganglionopathy, antibody-mediated hyperexcitability syndromes, and a host of medications. Particularly relevant to neurologic practice is the detection of postganglionic sudomotor deficits as a diagnostic marker of small fiber neuropathies. Extensive anhidrosis is important to recognize, as it not only correlates with symptoms of heat intolerance but may also place the patient at risk for heat stroke when under conditions of heat stress. Methods for assessing sudomotor dysfunction include the thermoregulatory sweat test, the quantitative sudomotor axon reflex test, silicone impressions, and the sympathetic skin response.
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May, Paul J., Wensi Sun, Nicholas F. Wright, and Jonathan T. Erichsen. "Pupillary light reflex circuits in the macaque monkey: the preganglionic Edinger–Westphal nucleus." Brain Structure and Function 225, no. 1 (December 24, 2019): 403–25. http://dx.doi.org/10.1007/s00429-019-02000-w.
Full textAbstract:
AbstractThe motor outflow for the pupillary light reflex originates in the preganglionic motoneuron subdivision of the Edinger–Westphal nucleus (EWpg), which also mediates lens accommodation. Despite their importance for vision, the morphology, ultrastructure and luminance-related inputs of these motoneurons have not been fully described in primates. In macaque monkeys, we labeled EWpg motoneurons from ciliary ganglion and orbital injections. Both approaches indicated preganglionic motoneurons occupy an EWpg organized as a unitary, ipsilateral cell column. When tracers were placed in the pretectal complex, labeled terminals targeted the ipsilateral EWpg and reached contralateral EWpg by crossing both above and below the cerebral aqueduct. They also terminated in the lateral visceral column, a ventrolateral periaqueductal gray region containing neurons projecting to the contralateral pretectum. Combining olivary pretectal and ciliary ganglion injections to determine whether a direct pupillary light reflex projection is present revealed a labeled motoneuron subpopulation that displayed close associations with labeled pretectal terminal boutons. Ultrastructurally, this subpopulation received synaptic contacts from labeled pretectal terminals that contained numerous clear spherical vesicles, suggesting excitation, and scattered dense-core vesicles, suggesting peptidergic co-transmitters. A variety of axon terminal classes, some of which may serve the near response, synapsed on preganglionic motoneurons. Quantitative analysis indicated that pupillary motoneurons receive more inhibitory inputs than lens motoneurons. To summarize, the pupillary light reflex circuit utilizes a monosynaptic, excitatory, bilateral pretectal projection to a distinct subpopulation of EWpg motoneurons. Furthermore, the interconnections between the lateral visceral column and olivary pretectal nucleus may provide pretectal cells with bilateral retinal fields.
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McDougall, Stuart J., and Michael C. Andresen. "Independent transmission of convergent visceral primary afferents in the solitary tract nucleus." Journal of Neurophysiology 109, no. 2 (January 15, 2013): 507–17. http://dx.doi.org/10.1152/jn.00726.2012.
Full textAbstract:
Cranial primary afferents from the viscera enter the brain at the solitary tract nucleus (NTS), where their information is integrated for homeostatic reflexes. The organization of sensory inputs is poorly understood, despite its critical impact on overall reflex performance characteristics. Single afferents from the solitary tract (ST) branch within NTS and make multiple contacts onto individual neurons. Many neurons receive more than one ST input. To assess the potential interaction between converging afferents and proximal branching near to second-order neurons, we probed near the recorded soma in horizontal slices from rats with focal electrodes and minimal shocks. Remote ST shocks evoked monosynaptic excitatory postsynaptic currents (EPSCs), and nearby focal shocks also activated monosynaptic EPSCs. We tested the timing and order of stimulation to determine whether focal shocks influenced ST responses and vice versa in single neurons. Focal-evoked EPSC response profiles closely resembled ST-EPSC characteristics. Mean synaptic jitters, failure rates, depression, and phenotypic segregation by capsaicin responsiveness were indistinguishable between focal and ST-evoked EPSCs. ST-EPSCs failed to affect focal-EPSCs within neurons, indicating that release sites and synaptic terminals were functionally independent and isolated from cross talk or neurotransmitter overflow. In only one instance, focal shocks intercepted and depleted the ST axon generating evoked EPSCs. Despite large numbers of functional contacts, multiple afferents do not appear to interact, and ST axon branches may be limited to close to the soma. Thus single or multiple primary afferents and their presynaptic active release sites act independently when they contact single second-order NTS neurons.
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Dewi Untari, Ni Komang Sri, Kurnia Kusumastuti, Guritno Suryokusumo, I. Ketut Sudiana, and Tedy Juliandhy. "Histological and Clinical Findings in Rabbits Sensitized with GM1 Ganglioside." Open Access Macedonian Journal of Medical Sciences 8, A (August 18, 2020): 801–5. http://dx.doi.org/10.3889/oamjms.2020.4871.
Full textAbstract:
BACKGROUND: Acute motor axonal neuropathy (AMAN) is a peripheral nerve disorder that attacks motor axons and occurs acutely. AMAN is one type of Guillain–Barre syndrome (GBS) which often attacks men of productive age. Until now, although patients have undergone intravenous immunoglobulin (IVIG) therapy and/or plasmapheresis, long-standing disability remains a problem. In Indonesia, the availability and cost of these therapies are constraints.
AIM: Our study aimed to find a proper animal model suitable for AMAN and can be executed in our institution, Naval Health Institute with a hope to find new therapeutic modalities in healing with AMAN.
METHODS: GM1 ganglioside immunized in New Zealand male white rabbits with complete Freund’s adjuvant, every 3 weeks until 20 weeks. We evaluated the effects GM1 ganglioside on body weight, functional score, and axon degeneration’s scale. Functional score was examined based on Tarlov’s. Hematoxylin-eosin was used to stain this slide.
RESULTS: Rabbits that being immunized with GM1 ganglioside experience a number of neurological signs and symptoms that resemble AMAN, that is, sluggish righting reflex, muscular weakness, flaccid hyper paralysis, and body weight loss. Pathological examination shows extensive degeneration of peripheral nerves, infiltration of macrophages, and perineuritis.
CONCLUSION: This histological and clinical findings support that this neuropathy is induced by an autoimmune response delivered by cells that respond to gangliosides.
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Takahashi, Yuzuru, Tatsuo Morinaga, Shin-Ichiro Nakamura, Kaoru Suseki, Kazuhisa Takahashi, and Yoshio Nakajima. "Neural connection between the ventral portion of the lumbar intervertebral disc and the groin skin." Journal of Neurosurgery 85, no. 2 (August 1996): 323–28. http://dx.doi.org/10.3171/jns.1996.85.2.0323.
Full textAbstract:
✓ This study was designed to investigate neural mechanisms of referred pain in lumbar intervertebral disc lesions. Patients with a degenerative disc in lower lumbar segments occasionally complain of groin pain, which cannot be explained anatomically as having a radicular origin. In rats pretreated with intravenous application of Evans blue dye, the dye extravasation appeared in the groin skin after application of capsaicin to the ventral portion of the L5–6 intervertebral disc. This response occurred even in rats with a sectioned L-5 spinal nerve and sympathetic trunks, but did not occur in rats with a sectioned genitofemoral nerve. Capsaicin topically applied to the sciatic nerve did not cause dye extravasation in the hindpaw. Therefore, groin dye extravasation was not due to a direct effect of capsaicin but, rather, presumably was caused by an “antidromic axon reflex” of dichotomizing C fibers or to a segmental sympathetic reflex causing vascular permeability. The present results indicate that the ventral portion of the lumbar discs is neurally connected to the groin skin via the upper (L-2) lumbar spinal nerves in rats. Groin pain coincident with low-back pain may be explained as referred pain, indicating that a lesion is present in the ventral portion of the lumbar intervertebral disc space.
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Carp, J. S., and J. R. Wolpaw. "Motoneuron plasticity underlying operantly conditioned decrease in primate H-reflex." Journal of Neurophysiology 72, no. 1 (July 1, 1994): 431–42. http://dx.doi.org/10.1152/jn.1994.72.1.431.
Full textAbstract:
1. Monkeys can gradually increase or decrease the size of the triceps surae H-reflex in response to an operant conditioning task. This conditioning modifies the spinal cord. To determine the location and nature of the spinal cord plasticity and define its role in the behavioral change (i.e., H-reflex increase or decrease) we have recorded intracellularly from triceps surae motoneurons in conditioned animals and compared the results with data from naive (i.e., unconditioned) animals. 2. Eleven monkeys (Macaca nemestrina, male) were exposed to the HRdown conditioning mode, in which reward occurred when H-reflex size in one leg (i.e., the trained leg) was below a criterion value. In six animals (5.1–8.2 kg) H-reflex size in the trained leg fell to 24–58% of its initial value, whereas in the other five animals (4.0–5.5 kg) it remained at 92–114% of its initial value. This outcome, which was in accord with recent data indicating that success in HRdown conditioning is age dependent, allowed comparison of intracellular data from successful HRdown animals with data from unsuccessful animals as well as with data from naive (i.e., unconditioned) animals. 3. Intracellular recordings were obtained from 221 triceps surae motoneurons on trained and control sides of successful and unsuccessful HRdown animals. Measurements included axonal conduction velocity, input resistance, time constant, electrotonic length, rheobase, firing threshold, afterhyperpolarization duration and amplitude, and composite homonymous and heteronymous excitatory postsynaptic potentials to peripheral nerve stimulation. Results were compared with data from 109 triceps surae motoneurons in naive animals. 4. Motoneurons from the trained side of successful HRdown animals had a significantly more positive average firing threshold (-52 vs. -55 mV) and a significantly lower average conduction velocity (67 vs. 71 m/s) than those from naive animals. In contrast, motoneurons from the trained side of unsuccessful HRdown animals were not significantly different from naive motoneurons. 5. These data are consistent with the hypothesis that operantly conditioned decrease in H-reflex size is due to a positive shift in motoneuron firing threshold and a consequent increase in the depolarization needed to reach that threshold. 6. The more positive firing threshold, if present in the axon as well as in the soma, could also account for the decreased conduction velocity observed in motoneurons from the trained side of successful animals.
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Sabatier, Manning J., Bao Ngoc To, Samuel Rose, Jennifer Nicolini, and Arthur W. English. "Chondroitinase ABC reduces time to muscle reinnervation and improves functional recovery after sciatic nerve transection in rats." Journal of Neurophysiology 107, no. 3 (February 2012): 747–57. http://dx.doi.org/10.1152/jn.00887.2011.
Full textAbstract:
Application of chondroitinase ABC (ChABC) to injured peripheral nerves improves axon regeneration, but it is not known whether functional recovery is also improved. Recordings of EMG activity [soleus (Sol) M response and H reflexes] evoked by nerve stimulation and of Sol and tibialis anterior (TA) EMG activity and hindlimb and foot kinematics during slope walking were made to determine whether ChABC treatment of the sciatic nerve at the time of transection improves functional recovery. Recovery of evoked EMG responses began as multiple small responses with a wide range of latencies that eventually coalesced into one or two more distinctive and consistent responses (the putative M response and the putative H reflex) in both groups. Both the initial evoked responses and the time course of their maturation returned sooner in the ChABC group than in the untreated (UT) group. The reinnervated Sol and TA were coactivated during treadmill locomotion during downslope, level, and upslope walking throughout the study period in both UT and ChABC-treated rats. By 10 wk after nerve transection and repair, locomotor activity in Sol, but not TA, had returned to its pretransection pattern. There was an increased reliance on central control of Sol activation across slopes for both groups as interpreted from elevated prestance Sol EMG activity that was no longer modulated with slope. Limb length and orientation during locomotion were similar to those observed prior to nerve injury during upslope walking only in the ChABC-treated rats. Thus treatment of cut nerves with ChABC leads to improvements in functional recovery.
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Walmsley, D., and P. G. Wiles. "Early loss of neurogenic inflammation in the human diabetic foot." Clinical Science 80, no. 6 (June 1, 1991): 605–10. http://dx.doi.org/10.1042/cs0800605.
Full textAbstract:
1. Neurogenic inflammation, mediated by nociceptor C fibres, is part of the acute neurovascular response to injury producing the axon reflex flare. Laser Doppler flowmetry was used to measure the flare response induced by the electrophoresis, at various current strengths, of a ring of acetylcholine solution into dorsal foot skin. 2. Nineteen control subjects and 52 long-duration insulin-dependent (Type 1) diabetic patients of similar age (20 without complications; 19 with laser-treated retinopathy; 13 with reduced vibration perception and retinopathy) were studied in order to investigate the possible attenuation of this defence mechanism in diabetes. 3. The maximal (1 mA) flare response [control median (interquartile range): 1.55 (1.16–2.06) arbitrary units] was reduced greatly in neuropathic patients [0.37 (0.24–0.66) arbitrary units; P ≤ 0.001 with respect to all other groups], especially those with a previous history of foot ulceration. The flare was also reduced in some patients with retinopathy alone [1.06 (0.56–1.27) arbitrary units; P < 0.005 with respect to control subjects]. 4. No rightward shift of the curve of hyperaemic response plotted against current strength was found, suggesting that the abnormal response was due to axonal loss rather than to dysfunction. 5. Neurogenic inflammation, mediated by small pain fibres, was markedly impaired in a group of diabetic patients at risk of foot ulceration. Furthermore, impairment of this nociceptor C fibre response can develop before clinical large-fibre neuropathy and could itself predispose to foot complications.
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Hodges, Gary J., Wojciech A. Kosiba, Kun Zhao, and John M. Johnson. "The involvement of heating rate and vasoconstrictor nerves in the cutaneous vasodilator response to skin warming." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 1 (January 2009): H51—H56. http://dx.doi.org/10.1152/ajpheart.00919.2008.
Full textAbstract:
Slow local skin heating (LH) causes vasodilator responses, some of which are dependent on sympathetic nerve function. It is not known, however, how the rate of LH affects either the sympathetic or the nonadrenergic components of the responses to LH and whether the adrenergic effects of LH depend on tonic sympathetic activity or whether LH stimulates transmitter release. In part 1, cutaneous vascular conductance (CVC) responses to slow and fast LH (+0.1° and +2°C/min) from 34° to 40°C were compared both at control sites and at sites pretreated with bretylium tosylate (BT; blocks transmitter release from adrenergic terminals). We confirmed, as previously found, the axon reflex (AR) response to slow LH to be blocked by BT ( P < 0.05). Pretreatment with BT reduced the AR only with fast LH. BT inhibited the peak vasodilation achieved with both rates of LH ( P < 0.05). Longer-term LH was associated with a slow fall in CVC, the classical “die away” phenomenon, at untreated sites ( P < 0.05) but not at BT-pretreated sites. Thus the LH-stimulated AR is only partially dependent on intact sympathetic function, and the “die away” phenomenon is dependent on such function. In part 2, we tested whether the conditions in part 1 (whole body and local skin temperatures of 34°C) completely suppressed sympathetic nerve activity. The infusion of BT by microdialysis did not change the CVC ( P > 0.05), suggesting the absence of tonic activity in those conditions and therefore that the adrenergic components of the responses in part 1 are via the stimulation of the transmitter release by LH.
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Barman, S. M., and G. L. Gebber. "Lateral tegmental field neurons of cat medulla: a source of basal activity of ventrolateral medullospinal sympathoexcitatory neurons." Journal of Neurophysiology 57, no. 5 (May 1, 1987): 1410–24. http://dx.doi.org/10.1152/jn.1987.57.5.1410.
Full textAbstract:
We tested the hypothesis that neurons of the lateral tegmental field (LTF) of the cat medulla exert their sympathoexcitatory actions over a pathway that includes rostral ventrolateral medullospinal neurons innervating the spinal intermediolateral nucleus (IML). Thirty-one LTF neurons with sympathetic nerve-related activity [as demonstrated with spike-triggered averaging of inferior cardiac postganglionic sympathetic nerve discharge (SND)] were antidromically activated by microstimulation of the rostral ventrolateral medulla (VLM). The threshold current required to elicit the longest latency antidromic response was increased when the stimulating microelectrode was moved to more dorsal or medial sites in the rostral medulla. This observation suggests that the axons of LTF neurons projected to the rostral VLM. The firing rate of LTF neurons with sympathetic nerve-related activity was decreased during baroreceptor reflex activation. This observation is consistent with the view that these neurons subserved a sympathoexcitatory function. Twenty-five VLM neurons with sympathetic nerve-related activity were synaptically activated by microstimulation of the LTF. The modal onset latency of synaptic excitation (25.6 +/- 2.6 ms) compared favorably with the difference (31 ms on the average) between the firing times of LTF and VLM neurons relative to the peak of the cardiac-related sympathetic nerve slow wave. The firing rate of these VLM neurons decreased during baroreceptor reflex activation. Of nine VLM neurons tested, seven were antidromically activated by microstimulation of the second thoracic (T2) IML. These data are consistent with the view that LTF neurons are a source of the basal discharge of VLM-spinal sympathoexcitatory neurons. Sixteen VLM neurons with sympathetic nerve-related activity were antidromically activated by microstimulation of both the LTF and the T2 IML. In some cases, LTF stimulation activated an axonal branch rather than the main axon. This was demonstrated using time-controlled collision of the VLM neuronal action potentials initiated by LTF and T2 IML stimulation. These data raise the possibility that individual VLM neurons influence SND by actions mediated at both spinal and supraspinal levels.
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Boutsiouki, Paraskevi, and Geraldine F. Clough. "Modulation of microvascular function following low-dose exposure to the organophosphorous compound malathion in human skin in vivo." Journal of Applied Physiology 97, no. 3 (September 2004): 1091–97. http://dx.doi.org/10.1152/japplphysiol.00123.2004.
Full textAbstract:
This study investigates whether malathion, a widely used organophosphate insecticide, has its effects on cutaneous vasculature in healthy human volunteers through its anticholinergic activity or through the modulation of other, noncholinergic pathways. Acute, low-dose exposure to malathion (10 mg/ml for 5 h under occlusive dressing) caused a significant increase in cutaneous blood flux, monitored by using laser-Doppler flowmetry and imaging. It had little effect on tissue levels of ACh, nitric oxide, and histamine assayed in dermal dialysate collected from malathion-exposed and control-treated skin. The duration of the cutaneous vascular response to exogenous ACh (2%) delivered by iontophoresis was significantly enhanced by preexposure to malathion, both <1 h after its removal and 24 h later ( P < 0.001). At <1 h, the time to 50% decay of the response was 24 ± 4 and 50 ± 8 min in control and malathion-treated skin, respectively. Malathion also enhanced the size and duration of the axon reflex-mediated vasoresponse to ACh. The increase in blood flux to malathion and the endothelium-mediated response to exogenous ACh, both in the presence and absence of malathion, were attenuated by pretreatment of the skin with atropine and local anesthesia ( P < 0.01). We conclude that short-term exposure to a single low dose of malathion causes prolonged modulation of the physiological function of the cutaneous vasculature and that this is, in part, through its action on acetylcholinesterase at both neuronal and nonneuronal sites.
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Barman, S. M. "Descending projections of hypothalamic neurons with sympathetic nerve-related activity." Journal of Neurophysiology 64, no. 3 (September 1, 1990): 1019–32. http://dx.doi.org/10.1152/jn.1990.64.3.1019.
Full textAbstract:
1. Spike-triggered averaging was used to identify 104 hypothalamic (HYP) neurons whose spontaneous or L-glutamate-induced action potentials were synchronized to inferior cardiac postganglionic-sympathetic nerve discharge (SND) in 39 pentobarbital sodium-anesthetized cats. Neurons were located primarily in the lateral hypothalamus but also in the posterior, dorsal, ventromedial, and anterior hypothalamus, as well as in the paraventricular region. Most neurons tested (41/60) were classified as sympathoexcitatory (SE) because their firing rate decreased during baroreceptor reflex activation. Because the firing rate of 15 neurons increased during the pressor response produced by aortic obstruction, they were classified as sympathoinhibitory (SI). The firing rate of the other four neurons tested was unaffected by baroreceptor reflex activation. 2. Microstimulation of the medullary lateral tegmental field (LTF; stereotaxic plane P10.5-P12, 2.3-3 mm lateral to the midline) antidromically activated 11 of 58 HYP neurons with sympathetic nerve-related activity, including seven SE neurons and one SI neuron. Antidromic mapping was used to trace the axonal trajectories of HYP neurons that were activated by LTF microstimulation. The results of these experiments suggested that the axons of eight of these neurons branched or terminated in the LTF. The data obtained from another series of experiments were consistent with the view that these HYP neurons excited LTF-SE neurons. LTF-SE neurons were synaptically activated by electrical stimulation of the posterior or lateral hypothalamus. This stimulus also increased SND. The modal onset latency (36 +/- 7.2 ms, mean +/- SE) of synaptic activation of LTF-SE neurons was similar to the onset latency (38 +/- 6.8 ms) of antidromic activation of HYP neurons by LTF microstimulation. These data support the view that LTF-SE neurons are involved in mediating HYP influences on SND. 3. Rostral ventrolateral medullary (RVLM)-SE neurons, including those whose axons projected to the thoracic intermediolateral nucleus (IML), also appear to be involved in mediating HYP-stimulus-induced increases in SND. HYP stimulation synaptically activated these neurons with a modal onset latency of 36 +/- 9.6 ms. Microstimulation of the region containing RVLM-SE neurons antidromically activated 16 of 60 HYP neurons with sympathetic nerve-related activity. The nine neurons tested were classified as SE. antidromic mapping revealed that RVLM microstimulation activated the main axon rather than an axonal branch or terminal of 9 of 12 of these HYP neurons. 4. Microstimulation of the mesencephalic periaqueductal gray (PAG) at stereotaxic planes A2-A3.5 antidromically activated 30 of 61 HYP neurons with sympathetic nerve-related activity, including 13 SE neurons and three SI neurons.(ABSTRACT TRUNCATED AT 400 WORDS)
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Tartas, M., P. Bouyé, A. Koïtka, V. Jaquinandi, L. Tan, J. L. Saumet, and P. Abraham. "Cathodal current-induced vasodilation to single application and the amplified response to repeated application in humans rely on aspirin-sensitive mechanisms." Journal of Applied Physiology 99, no. 4 (October 2005): 1538–44. http://dx.doi.org/10.1152/japplphysiol.00258.2005.
Full textAbstract:
Assumed to rely on an axon reflex, the current-induced vasodilation (CIV) interferes with the microvascular response to iontophoretic drug delivery. Mechanisms resulting in CIV are likely different at the anode and at the cathode. While studies have been conducted to understand anodal CIV, little information is available on cathodal CIV. The present study investigates CIV observed following 0.1-mA cathodal applications on forearms of healthy volunteers and the possible mechanisms involved. Results are expressed in percentage of the cutaneous heat-induced maximal vascular conductance [%MVC (means ± SE)]. 1) The amplitude of CIV was proportional to the duration of cathodal currents for periods of <1 min: r = 0.99. 2) Two current applications of 10 s, with 10-min interstimulation interval, induced a higher peak value of CIV (79.1 ± 8.6% MVC) than the one obtained with all-at-once 20-s current application (39.5 ± 4.3% MVC, P < 0.05). This amplified vascular response due to segmental application was observed for all tested interstimulation intervals (up to 40 min). 3) Two hours and 3 days following pretreatment with 1-g oral aspirin, the CIV observed following cathodal application, as well as the difference of cathodal CIV amplitude between all-at-once and segmented applications, were reduced. These findings suggest a role of prostaglandins, not only released from endothelial or smooth muscle cells, as direct vasodilator and/or as a sensitizer. Thus aspirin pretreatment could be used to decrease CIV resulting from all-at-once and repeated cathodal application and facilitate the study of the specific vascular effect induced by the drug delivered.
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Crossman, D. C., S. D. Brain, and R. W. Fuller. "Potent vasoactive properties of endothelin 1 in human skin." Journal of Applied Physiology 70, no. 1 (January 1, 1991): 260–66. http://dx.doi.org/10.1152/jappl.1991.70.1.260.
Full textAbstract:
The effect of the endothelial cell-derived peptide endothelin 1 was investigated in human skin. Intradermal injection of endothelin 1 (1–100 pmol) caused a dose-dependent area of pallor that was associated with a significant reduction in basal skin blood flow, measured by laser-Doppler blood flowmeter (with 1 pmol endothelin, P = 0.012, analysis of variance). The coadministration of endothelin 1 (1–100 pmol) with the neuropeptide vasodilator calcitonin gene-related peptide (CGRP) inhibited the vasodilator response to CGRP (10 pmol) by up to 82.7 +/- 9.2% (with 100 pmol endothelin, P less than 0.001). The response of the prostanoid vasodilator prostaglandin E2 (10 pmol) was inhibited by endothelin in a similar manner. In addition to the vasoconstrictor effects, endothelin 1 produced a dose-dependent flare that surrounded the area of pallor, and this was associated with a significant increase in blood flow (P less than 0.05) within the flare area. The H1 antagonist terfenadine (120 mg po) significantly reduced the flare area associated with endothelin 1: flare 5 min after intradermal endothelin (10 pmol, placebo treated), 668 +/- 405 mm2; terfenadine treated, 201 +/- 257 mm2 (P less than 0.05). The flare was also significantly attenuated when endothelin (10 pmol) was injected into local anesthetic-treated skin. Thus intradermal injection of endothelin in humans causes long-lasting vasoconstriction at the site of injection and a surrounding flare. Results suggest that the flare component is partially histamine dependent and the result of an axon reflex. This study demonstrates the potent activity of endothelin in human skin. It is possible that endothelin could be relevant to the local response of skin to injury.
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Hodges, Gary J., Wojciech A. Kosiba, Kun Zhao, and John M. Johnson. "The involvement of norepinephrine, neuropeptide Y, and nitric oxide in the cutaneous vasodilator response to local heating in humans." Journal of Applied Physiology 105, no. 1 (July 2008): 233–40. http://dx.doi.org/10.1152/japplphysiol.90412.2008.
Full textAbstract:
Presynaptic blockade of cutaneous vasoconstrictor nerves (VCN) abolishes the axon reflex (AR) during slow local heating (SLH) and reduces the vasodilator response. In a two-part study, forearm sites were instrumented with microdialysis fibers, local heaters, and laser-Doppler flow probes. Sites were locally heated from 33 to 40°C over 70 min. In part 1, we tested whether this effect of VCN acted via nitric oxide synthase (NOS). In five subjects, treatments were as follows: 1) untreated; 2) bretylium, preventing neurotransmitter release; 3) NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS; and 4) combined bretylium + l-NAME. At treated sites, the AR was absent, and there was an attenuation of the ultimate vasodilation ( P < 0.05), which was not different among those sites ( P > 0.05). In part 2, we tested whether norepinephrine and/or neuropeptide Y is involved in the cutaneous vasodilator response to SLH. In seven subjects, treatments were as follows: 1) untreated; 2) propranolol and yohimbine to antagonize α- and β-receptors; 3) BIBP-3226 to antagonize Y1 receptors; and 4) combined propranolol + yohimbine + BIBP-3226. Treatment with propranolol + yohimbine or BIBP-3226 significantly increased the temperature at which AR occurred ( n = 4) or abolished it ( n = 3). The combination treatment consistently eliminated it. Importantly, ultimate vasodilation with SLH at the treated sites was significantly ( P < 0.05) less than at the control. These data suggest that norepinephrine and neuropeptide Y are important in the initiation of the AR and for achieving a complete vasodilator response. Since VCN and NOS blockade in combination do not have an inhibition greater than either alone, these data suggest that VCN promote heat-induced vasodilation via a nitric oxide-dependent mechanism.
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Hassan, A. A. K., G. Rayman, and J. E. Tooke. "Effect of indirect heating on the postural control of skin blood flow in the human foot." Clinical Science 70, no. 6 (June 1, 1986): 577–82. http://dx.doi.org/10.1042/cs0700577.
Full textAbstract:
1. It has been shown in previous studies that skin blood flow in the human foot falls when the extremity is placed below heart level, owing to an increase in precapillary resistance that is probably mediated by a local sympathetic axon reflex or a myogenic response. 2. In order to clarify the influence of the central thermoregulatory mechanisms on this local postural vasoconstrictor response, 12 normal male subjects were studied under standardized conditions, at rest and during heating of the trunk with an electric blanket. 3. Skin blood flow was measured before and during body heating using laser Doppler flowmetry with the foot maintained at heart level and placed passively 50 cm below the heart. 4. Skin blood flow and skin temperature were determined at two sites: (a) the plantar surface of the big toe, an area with a relatively large number of arteriovenous anastomoses, and (b) the dorsum of the same foot, where these anastomoses are few or absent. 5. When the foot was placed in the dependent position, skin blood flow recorded in the dorsum of the foot during indirect heating fell to a level similar to that achieved before heating. In contrast, indirect heating greatly diminished the postural fall in skin blood flow recorded in the plantar surface of the big toe. 6. In conclusion, the partial release of sympathetic vasoconstrictor tone associated with indirect heating appears to over-ride the local postural control of cutaneous vascular tone in areas where arteriovenous anastomoses are relatively numerous.
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Dulin, M. F., I. Steffensen, C. E. Morris, and E. T. Walters. "Recovery of function, peripheral sensitization and sensory neurone activation by novel pathways following axonal injury in Aplysia californica." Journal of Experimental Biology 198, no. 10 (October 1, 1995): 2055–66. http://dx.doi.org/10.1242/jeb.198.10.2055.
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Recovery of behavioural and sensory function was examined following unilateral pedal nerve crush in Aplysia californica. Nerve crush that transected all axons connecting the tail to the central nervous system (CNS) eliminated the ipsilateral tail-evoked siphon reflex, whose sensory input travels in the crushed tail nerve (p9). The first reliable signs of recovery of this reflex were observed within 1 week, and most animals displayed tail-evoked siphon responses within 2 weeks. Wide-dynamic-range mechanosensory neurons with somata in the ventrocaudal (VC) cluster of the ipsilateral pleural ganglion exhibited a few receptive fields (RFs) on the tail 3 weeks after unilateral pedal nerve crush, indicating that the RFs had either regenerated or been reconnected to the central somata. These RFs were smaller and sensitized compared with corresponding RFs on the contralateral, uncrushed side. Centrally conducted axon responses of VC sensory neurones to electrical stimulation distal to the nerve crush site did not reappear until at least 10 days after the crush. Because the crush site was much closer to the CNS than to the tail, the failure of axon responses to be restored earlier than the behavioural responses indicates that early stages of reflex recovery are not due to regeneration of VC sensory neurone axons into the tail. Following nerve crush, VC sensory neurones often could be activated by stimulating central connectives or peripheral nerves that do not normally contain the sensory neurone's axons. These results suggest that recovery of behavioral function after nerve injury involves complex mechanisms, including regenerative growth of axotomized VC sensory neurones, sensitization of regenerating RFs and sprouting of VC sensory neurone fibres within the CNS. Furthermore, the rapidity of behavioural recovery indicates that its initial phases are mediated by additional mechanisms, perhaps centripetal regeneration of unidentified sensory neurones having peripheral somata, or transient reconnection of proximal and distal stumps of axotomized VC cells.
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Stevens, M. J., M. E. Edmonds, S. L. E. Douglas, and P. J. Watkins. "Influence of Neuropathy on the Microvascular Response to Local Heating in the Human Diabetic Foot." Clinical Science 80, no. 3 (March 1, 1991): 249–56. http://dx.doi.org/10.1042/cs0800249.
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1. The diabetic neuropathic foot exhibits excess arteriovenous anastomotic shunt flow due to a reduced sympathetic vasoconstrictor tone. Local axon reflexes (mediating postural vasoconstriction, for example) are preserved even in severe diabetic neuropathy. This excess shunt flow and its local neurogenic control may be important in the development of complications of the neuropathic limb. 2. The response of arteriovenous anastomoses to local heating was assessed in 13 diabetic patients with neuropathy (12 insulin-dependent), 10 diabetic control patients (seven insulin-dependent) and 10 normal control subjects. The aim was to study the local reflex control of arteriovenous flow when central sympathetic tone had been largely removed. 3. The change in skin blood flow on local heating to 44°C was measured by using a laser Doppler flowmeter in standard environmental conditions with the foot at heart level. Two sites were assessed: (i) the plantar surface of the great toe (a site in which skin blood flow is dominated by arteriovenous shunt flow) and (ii) the dorsum of the foot (a site without anastomotic flow). 4. It was found that when heat was applied to the plantar surface of the great toe in the diabetic patients with neuropathy a paradoxical decrease in flow through arteriovenous anastomoses occurred, flow declining to 65% (P < 0.05) of its resting value. This could be compared with an increase in flow over the same time period of 262% and 228% (P < 0.01) in diabetic control patients and normal subjects, respectively. When the foot dorsum was heated flow increased in a similar fashion in all patient groups, and a decline in flow was not observed. 5. Peak flow at the great toe was significantly lower in the diabetic patients with neuropathy compared with both the diabetic control patients and the normal subjects [23.68 (44.64) flow units versus 57.0 (43.92) flow units and 76.32 (40.88) flow units, respectively, medians and interquartile ranges, P < 0.02]. 6. Thus we have demonstrated that in the presence of neuropathy local heating of the toe pulp may produce (i) a paradoxical fall in skin blood flow and (ii) a greatly reduced peak skin blood flow. The importance of this abnormal vascular control in the pathogenesis of complications of the neuropathic limb has now to be determined.
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Sasano, T., S. Kuriwada, N. Shoji, D. Sanjo, H. Izumi, and K. Karita. "Axon Reflex Vasodilatation in Cat Dental Pulp Elicited by Noxious Stimulation of the Gingiva." Journal of Dental Research 73, no. 12 (December 1994): 1797–802. http://dx.doi.org/10.1177/00220345940730120201.
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Antidromic stimulation of sensory nerves has been shown to increase blood flow in the tissue they innervate. This study was designed to determine if antidromic vasomotor responses occur in feline dental pulp and if they are mediated by branched axons supplying both tooth pulp and gingiva. Dynamic changes in pulpal blood flow (PBF) elicited by electrical stimulation, pinching, heating, and capsaicin application to the gingivae were investigated in cat mandibular canine teeth by means of Laser Doppler Velocimetry. All inferior alveolar nerve bundles and the cervical sympathetic trunk had been previously sectioned to avoid the occurrence of brainstem reflexes, e.g., somato-autonomic vasomotor reflexes. Increases in PBF were observed in seven out of 12 cats when a restricted gingival area adjacent to the canine teeth was stimulated as described, but the increases were abolished after the sensitive gingival area was painted with lidocaine jelly, a surface anesthetic. These vasodilator responses, remarkably reduced following repeated application of 30 mM of capsaicin, are considered to be induced via antidromic activation of capsaicin-sensitive nociceptive nerve fibers, presumably by axon reflex mechanisms, suggesting that nerve terminals supplying the gingiva originate from parent axons which have collaterals that innervate the canine tooth pulp.
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JOO, HANNAH R., BETH B. PETERSON, DENNIS M. DACEY, SAMER HATTAR, and SHIH-KUO CHEN. "Recurrent axon collaterals of intrinsically photosensitive retinal ganglion cells." Visual Neuroscience 30, no. 4 (July 2013): 175–82. http://dx.doi.org/10.1017/s0952523813000199.
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AbstractRetinal ganglion cells (RGCs), the output neurons of the retina, have axons that project via the optic nerve to diverse targets in the brain. Typically, RGC axons do not branch before exiting the retina and thus do not provide it with synaptic feedback. Although a small subset of RGCs with intraretinal axon collaterals has been previously observed in human, monkey, cat, and turtle, their function remains unknown. A small, more recently identified population of RGCs expresses the photopigment melanopsin. These intrinsically photosensitive retinal ganglion cells (ipRGCs) transmit an irradiance-coding signal to visual nuclei in the brain, contributing both to image-forming vision and to several nonimage-forming functions, including circadian photoentrainment and the pupillary light reflex. In this study, using melanopsin immunolabeling in monkey and a genetic method to sparsely label the melanopsin cells in mouse, we show that a subgroup of ipRGCs have axons that branch en route to the optic disc, forming intraretinal axon collaterals that terminate in the inner plexiform layer of the retina. The previously described collateral-bearing population identified by intracellular dye injection is anatomically indistinguishable from the collateral-bearing melanopsin cells identified here, suggesting they are a subset of the melanopsin-expressing RGC type and may therefore share its functional properties. Identification of an anatomically distinct subpopulation in mouse, monkey, and human suggests this pathway may be conserved in these and other species (turtle and cat) with intraretinal axon collaterals. We speculate that ipRGC axon collaterals constitute a likely synaptic pathway for feedback of an irradiance signal to modulate retinal light responses.
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Bullinger, Katie L., Paul Nardelli, Martin J. Pinter, Francisco J. Alvarez, and Timothy C. Cope. "Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. II. Loss of functional connectivity with motoneurons." Journal of Neurophysiology 106, no. 5 (November 2011): 2471–85. http://dx.doi.org/10.1152/jn.01097.2010.
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Regeneration of a cut muscle nerve fails to restore the stretch reflex, and the companion paper to this article [Alvarez FJ, Titus-Mitchell HE, Bullinger KL, Kraszpulski M, Nardelli P, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01095.2010] suggests an important central contribution from substantial and persistent disassembly of synapses between regenerated primary afferents and motoneurons. In the present study we tested for physiological correlates of synaptic disruption. Anesthetized adult rats were studied 6 mo or more after a muscle nerve was severed and surgically rejoined. We recorded action potentials (spikes) from individual muscle afferents classified as IA like (*IA) by several criteria and tested for their capacity to produce excitatory postsynaptic potentials (EPSPs) in homonymous motoneurons, using spike-triggered averaging (STA). Nearly every paired recording from a *IA afferent and homonymous motoneuron (93%) produced a STA EPSP in normal rats, but that percentage was only 17% in rats with regenerated nerves. In addition, the number of motoneurons that produced aggregate excitatory stretch synaptic potentials (eSSPs) in response to stretch of the reinnervated muscle was reduced from 100% normally to 60% after nerve regeneration. The decline in functional connectivity was not attributable to synaptic depression, which returned to its normally low level after regeneration. From these findings and those in the companion paper, we put forward a model in which synaptic excitation of motoneurons by muscle stretch is reduced not only by misguided axon regeneration that reconnects afferents to the wrong receptor type but also by retraction of synapses with motoneurons by spindle afferents that successfully reconnect with spindle receptors in the periphery.
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Mack, Gary W. "A model for in vivo analysis of sudomotor sympathetic C-fiber activation and human sweat gland output." Journal of Applied Physiology 123, no. 2 (August 1, 2017): 317–25. http://dx.doi.org/10.1152/japplphysiol.01070.2016.
Full textAbstract:
Quantitative assessment of small-fiber peripheral neuropathy often involves an evaluation of the interaction between the C-fiber sudomotor nerve and local sweat rate (SR). Typically, some sort of quantitative sudomotor axon reflex test (QSART) is performed to aid in diagnosing small-fiber dysfunction. The currently used QSART demonstrates only moderate test-retest reliability and therefore limits its usefulness in tracking small-fiber dysfunction. A new experimental model to examine small C-fiber function in the skin using intradermal electrical stimulation and simultaneous monitoring of SR is proposed. Using intradermal electrical stimulation (1.5 and 2.5 mA) and varying stimulus frequency from 0.2 to 64 Hz, a quantitative relationship between the area under the SR–time curve and log10 stimulus frequency is modeled using a four-parameter logistic equation, providing the following parameters: baseline, plateau, EC50, and Hill slope. The model has good to excellent repeatability within the same day (ICC = 0.98), on different days at the same skin site (ICC = 0.80), and when comparing two different skin sites (ICC = 0.78) with a small bias estimate and the line of identity always lying within the 95% limits of agreement. Atropine sulfate (0.1 mg/ml) blocked 90 ± 5% of the electrically induced sweating. Overall, the model provides control over sudomotor nerve activity and a quantitative assessment of SR. Finally, the ability to reproduce the quantitative stimulus-response curve on different days allows for a robust assessment of the relationship between the activation of a sympathetic C-fiber and local SR. NEW & NOTEWORTHY A model for quantitative assessment of C-fiber function in human skin using intradermal electrical stimulation and local sweat rate measurements has been developed. This new electrically induced sweating model is nonpainful and allows for a complete stimulus-response curve plotting the area under the local sweat rate-time curve vs. the log10 stimulus frequency. The model has good reproducibility and should provide a means of assessing the progression of small C-fiber peripheral neuropathy in humans.
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Gordon, Tessa. "The role of neurotrophic factors in nerve regeneration." Neurosurgical Focus 26, no. 2 (February 2009): E3. http://dx.doi.org/10.3171/foc.2009.26.2.e3.
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This review considers the 2 sources of neurotrophic factors in the peripheral nervous system (PNS), the neurons and the nonneuronal cells in the denervated distal nerve stumps, and their role in axon regeneration. Morphological assessment of regenerative success in response to administration of exogenous growth factors after nerve injury and repair has indicated a role of the endogenous neurotrophic factors from Schwann cells in the distal nerve stump. However, the increased number of axons may reflect more neurons regenerating their axons and/or increased numbers of axon sprouts from the same number of neurons. Using fluorescent dyes to count neurons that regenerated their axons across a suture site and into distal nerve stumps, brain-derived neurotrophic factor (BDNF) and glial cell–derived neurotrophic factor (GDNF) were found not to increase the number of neurons that regenerated their axons after immediate nerve repair. Nevertheless, the factors did reverse the deleterious effect of delayed nerve repair, indicating that the axons that regenerate into the distal nerve stump normally have access to sufficient levels of endogenous neurotrophic factors to sustain their regeneration, while neurons that do not have access to these factors require exogenous factors to sustain axon regeneration. Neurons upregulate neurotrophic factors after axotomy. The upregulation is normally slow, beginning after 7 days and occurring in association with a protracted period of axonal regeneration in which axons grow out from the proximal nerve stump across a suture site over a period of 1 month in rodents. This staggered axon regeneration across the suture site is accelerated by a 1-hour period of low-frequency electrical stimulation that simultaneously accelerates the expression of BDNF and its trkB receptor in the neurons. Elevation of the level of BDNF after 2 days to > 3 times that found in unstimulated neurons was accompanied by elevation of the level of cAMP and followed by accelerated upregulation of growth-associated genes, tubulin, actin, and GAP-43 and downregulation of neurofilament protein. Elevation of cAMP levels via rolipram inhibition of phosphodiesterase 4 mimicked the effect of the low-frequency electrical stimulation. In conclusion, the enhanced upregulation of neurotrophic factors in the electrically stimulated axotomized neurons accelerates axon outgrowth into the distal nerve stumps where endogenous sources of growth factors in the Schwann cells support the regeneration of the axons toward the denervated targets. The findings provide strong support for endogenous neurotrophic factors of axotomized neurons and of denervated Schwann cells playing a critical role in supporting axon regeneration in the PNS.
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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.
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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.
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Fan, Wei, and Michael C. Andresen. "Differential frequency-dependent reflex integration of myelinated and nonmyelinated rat aortic baroreceptors." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 2 (August 1, 1998): H632—H640. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h632.
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Electrical activation of myelinated (A type) and nonmyelinated (C type) baroreceptor axons (BR) in aortic depressor nerve (ADN) evoked baroreflex changes in mean arterial pressure (MAP) in chloralose-urethan-anesthetized rats. Low stimulation intensities (<3 V) activated only A-type BR electroneurograms (ENG). A-type selective stimulus trains required minimum frequencies >10 Hz to evoke reflex MAP decreases, and the largest MAP responses occurred at 50 Hz and higher. In contrast, high stimulation intensities (18–20 V) maximally activated two volleys in ADN ENG corresponding to A- and C-type BR volleys. High-intensity trains decreased MAP at low frequency (1 Hz) and largest reflex responses at ≥5 Hz. Capsaicin (Cap) applied periaxonally to ADN selectively blocked C-type ENG volleys but not A-type volleys. Reflex curves with supramaximal intensity during Cap were indistinguishable from the pre-Cap, low-intensity baroreflexes. In comparison, vagus ENG showed graded Cap block of the C-fiber volley (ED50 = 200 nM) without significant attenuation of the A-type volley below 1 μM. However, 100 μM Cap blocked conduction in all myelinated vagal axons as well as C-type axons. Thus Cap is selective for sensory C-type axons only at low micromolar concentrations. Myelinated and nonmyelinated arterial BR evoke characteristically different frequency-response reflex relations that suggest distinct differences in sensory information processing mechanisms.