State-Dependent GABAergic Inhibition of Sciatic Nerve-Evoked Responses of Dorsal Spinocerebellar Tract Neurons

2004 ◽  
Vol 92 (3) ◽  
pp. 1479-1490 ◽  
Author(s):  
Niwat Taepavarapruk ◽  
Shelly A. McErlane ◽  
Angela Chan ◽  
Sylvia Chow ◽  
Liz Fabian ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Eye Movement ◽  
The State ◽  
Response Magnitude ◽  
Evoked Responses ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Spike Response ◽  
Spinocerebellar Tract

Peripheral nerve-evoked potentials recorded in the cerebellum 35 yr ago inferred that sensory transmission via the dorsal spinocerebellar tract (DSCT) is reduced occasionally and only during eye movements of active sleep compared with wakefulness or quiet sleep. A reduction or withdrawal of primary afferent input and/or ongoing inhibition of individual lumbar DSCT neurons may underlie this occurrence. This study distinguished between these possibilities by examining whether peripheral nerve-evoked responses recorded from individual DSCT neurons are suppressed specifically during active sleep, and if so, whether GABA mediates this phenomenon. Synaptic responses to threshold stimuli applied to the sciatic nerve were characterized by a single spike response at short latency and/or a longer latency burst of action potentials. During the state of quiet wakefulness, response magnitude did not differ from that observed during quiet sleep. During active sleep, short and long latency responses were suppressed by 26 and 14%, respectively, and returned to pre-active sleep levels following awakening from active sleep. Sciatic nerve-evoked early and late responses were further analyzed in a paired fashion around computer-tagged eye movement events that hallmark the state of active sleep. Response magnitude was suppressed by 14.4 and 11.5%, respectively, during eye movement events of active sleep. The GABAA antagonist bicuculline, applied juxtacellularly by microiontophoresis, abolished response suppression during non–eye movement periods and eye movement events of active sleep. In conclusion, synaptic transmission via DSCT neurons is inhibited by GABA tonically during non–eye movement periods and phasically during eye movement events of active sleep.

Apneic Spells and Sleep States in Preterm Infants

PEDIATRICS ◽  
1976 ◽  
Vol 57 (1) ◽  
pp. 142-147
Author(s):  
M. Gabriel ◽  
M. Albani ◽  
F. J. Schulte
Keyword(s):  
Nervous System ◽  
Eye Movement ◽  
Preterm Infants ◽  
Rem Sleep ◽  
Synaptic Connections ◽  
Spinal Motoneurons ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Recording Technique ◽  
Polygraphic Recording

The incidence of apneic spells during different sleep states, active sleep, quiet sleep, and undifferentiated sleep was determined in eight preterm infants of 30 to 35 weeks' conceptional age, by means of a polygraphic recording technique. They were free of perinatal and postnatal complications other than apnea. During their active or rapid eye movement (REM) sleep they showed significantly more apneic episodes which were also longer lasting and they were accompanied by bradycardia of a greater severity. The organization of the immature nervous system with a preponderance of inhibitory synaptic connections and the additional inhibition of spinal motoneurons during REM sleep are likely to be the cause of apneic spells in otherwise "normal" preterm infants.

Spinal evoked response in the cat

1975 ◽  
Vol 43 (3) ◽  
pp. 329-336 ◽  
Author(s):  
Robert J. Sarnowski ◽  
Roger Q. Cracco ◽  
Harold B. Vogel ◽  
Fred Mount
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Nerve Stimulation ◽  
Nerve Fibers ◽  
Evoked Responses ◽  
Afferent Pathways ◽  
Content Type ◽  
Sciatic Nerve Stimulation ◽  
Fine Print

✓ Summated evoked potentials to sciatic nerve stimulation were recorded from surface electrodes placed over the spine of cats. The response progressively increased in latency rostrally. It was largest and most complex in configuration in leads placed over the caudal spinal cord where sciatic nerve roots enter and begin to ascend the cord. The conduction velocity of the response was about 90 m/sec from rostral sacral to cervical regions. A comparison of surface-recorded evoked responses to stimulation of the sural nerve, the nerve to the medial head of the gastrocnemius muscle and the sciatic nerve suggest that the peripheral nerve fibers that mediate the response to sciatic nerve stimulation are primarily muscle nerve afferents. In surface, lamina, and durai recordings made over similar segmental levels, the response to sciatic nerve stimulation progressively increased in amplitude, duration, and wave form complexity from surface to depth. Failure of transmission across complete cord transections was demonstrated. Results in preparations with partial cord sections suggest that the surface-recorded response is mediated by multiple spinal cord afferent pathways which are situated primarily ipsilateral to the stimulated peripheral nerve. The data indicate that summated evoked responses arising in spinal cord afferent pathways can be recorded from surface-recording electrodes in cats. They suggest that this animal model may prove useful in the study of certain aspects of spinal cord pathology.

Facilitated migration of cells from a transected peripheral nerve over collagen fibers: in vivo observations

1989 ◽  
Vol 47 ◽  
pp. 888-889
Author(s):  
Arthur J. Wasserman ◽  
Azam Rizvi ◽  
George Zazanis ◽  
Frederick H. Silver
Keyword(s):  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Collagen Gel ◽  
Collagen Fibers ◽  
Control Group ◽  
Guide Tube ◽  
Sprague Dawley ◽  
Silicone Tube ◽  
Thin Sections

In cases of peripheral nerve damage the gap between proximal and distal stumps can be closed by suturing the ends together, using a nerve graft, or by nerve tubulization. Suturing allows regeneration but does not prevent formation of painful neuromas which adhere to adjacent tissues. Autografts are not reported to be as good as tubulization and require a second surgical site with additional risks and complications. Tubulization involves implanting a nerve guide tube that will provide a stable environment for axon proliferation while simultaneously preventing formation of fibrous scar tissue. Supplementing tubes with a collagen gel or collagen plus extracellular matrix factors is reported to increase axon proliferation when compared to controls. But there is no information regarding the use of collagen fibers to guide nerve cell migration through a tube. This communication reports ultrastructural observations on rat sciatic nerve regeneration through a silicone nerve stent containing crosslinked collagen fibers.Collagen fibers were prepared as described previously. The fibers were threaded through a silicone tube to form a central plug. One cm segments of sciatic nerve were excised from Sprague Dawley rats. A control group of rats received a silicone tube implant without collagen while an experimental group received the silicone tube containing a collagen fiber plug. At 4 and 6 weeks postoperatively, the implants were removed and fixed in 2.5% glutaraldehyde buffered by 0.1 M cacodylate containing 1.5 mM CaCl2 and balanced by 0.1 M sucrose. The explants were post-fixed in 1% OSO4, block stained in 1% uranyl acetate, dehydrated and embedded in Epon. Axons were counted on montages prepared at a total magnification of 1700x. Montages were viewed through a dissecting microscope. Thin sections were sampled from the proximal, middle and distal regions of regenerating sciatic plugs.

Averaged Evoked Responses and Loudness: Analysis of Response Estimates

1968 ◽  
Vol 11 (2) ◽  
pp. 334-342 ◽  
Author(s):  
Gretchen B. Henry ◽  
Donald C. Teas
Keyword(s):  
Noise Burst ◽  
Response Magnitude ◽  
Evoked Responses ◽  
Maximum Estimate

Averaged evoked responses to noise burst signals at six sensation levels were obtained in three experimental contexts and compared on the basis of response magnitude. No significant effects were found related to context; systematic differences were found, however, within the ensemble of responses making up the average. These differences suggest that the maximum estimate of response magnitude may be contained in the first few responses to a series of stimuli.

Individual mechanisms underlying peripheral nerve damage when exposed to metallic mercury

2020 ◽  
Vol 60 (12) ◽  
pp. 918-924
Author(s):  
Dina V. Rusanova ◽  
Oleg L. Lakhman ◽  
Galina M. Bodienkova ◽  
Irina V. Kudaeva ◽  
Natalya G. Kuptsova
Keyword(s):  
Peripheral Nerve ◽  
Peripheral Nerves ◽  
Blood Circulation ◽  
The State ◽  
Contact Period ◽  
Peripheral Nerve Damage ◽  
Demyelinating Disorders ◽  
Peripheral Blood Circulation ◽  
Antibodies To Dna

Introduction. There is a lack of knowledge of the pathophysiological mechanisms that form peripheral nerve disorders in mercury lesions of professional origin. The study aims to reveal the mechanisms underlying peripheral nerve damage in the long-term post-contact period of chronic mercury intoxication (CMI). Materials and methods. Fifty-one people had the diagnosis of a long-term period of CMI. The post-contact period was 8.5±2.6 years. The authors compared the results with a control group of 26 healthy men who had no contact with toxic substances. Stimulating electroneuromyography was performed. We studied the body systems that could contribute to the formation of disorders in the peripheral nerves. Changes in peripheral hemodynamics were studied using reovasography. The content of autoantibodies, neuron-specific enolase, serotonin, histamine, catecholamines (epinephrine, dopamine), metanephrine, and neurotrophin-3 was reviewed. The content of ceruloplasmin, secondary products of lipid peroxidation processes, reduced glutathione, the activity of superoxide dismutase and the content of nitric oxide levels were determined. Results. The study established pathogenetic structural links of peripheral nerve disorders. The autoimmune process's role was to increase the range of antibodies to the MAG protein and increase the level of antibodies to DNA. Violations of elastic-tonic properties of peripheral vessels could be associated with the functional state of motor axons. The increased content of neurotransmitters is related to the state of peripheral blood circulation; the most pronounced changes were on the legs, which could contribute to the occurrence and maintenance of vasoconstriction. The role of oxidative stress in the formation of demyelinating disorders in patients' peripheral nerves in the long-term period of CRI is possible. Conclusion. Neuroimmunological processes has an essential role in the development of peripheral nerve demyelination was shown, which consists in an increase in the content of antibodies to the MAG protein expressed on Schwann cells of peripheral nerves and in an increase in the level of antibodies to DNA involved in the formation of demyelinating changes when exposed to metallic mercury. The revealed pathological changes in the state of the peripheral blood circulation, characterized by a violation of the vessels' elastic-tonic properties, leading to demyelination of motor axons in patients in the long-term period of CMI. The increased content of neurotransmitters in the examined is of great importance in the state of peripheral circulation. Pronounced changes in blood circulation are established on the lower extremities, which may be associated with the predominance of α-adrenergic receptors in the arterial bed and may contribute to the occurrence and maintenance of vasoconstriction in the legs. The relationship between changes in indicators of oxidative stress, consisting of a decrease in the value of superoxide dismutase and reduced glutathione, and the formation of demyelinating disorders of peripheral nerves in patients in the long-term period of CMI has been proved.

Changes in Crossed Spinal Reflexes After Peripheral Nerve Injury and Repair

2002 ◽  
Vol 87 (4) ◽  
pp. 1763-1771 ◽  
Author(s):  
Antoni Valero-Cabré ◽  
Xavier Navarro
Keyword(s):  
Sciatic Nerve ◽  
Action Potential ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Tibialis Anterior ◽  
Tibial Nerve ◽  
Spinal Reflexes ◽  
Injury And Repair

We investigated the changes induced in crossed extensor reflex responses after peripheral nerve injury and repair in the rat. Adults rats were submitted to non repaired sciatic nerve crush (CRH, n = 9), section repaired by either aligned epineurial suture (CS, n = 11) or silicone tube (SIL4, n = 13), and 8 mm resection repaired by tubulization (SIL8, n = 12). To assess reinnervation, the sciatic nerve was stimulated proximal to the injury site, and the evoked compound muscle action potential (M and H waves) from tibialis anterior and plantar muscles and nerve action potential (CNAP) from the tibial nerve and the 4th digital nerve were recorded at monthly intervals for 3 mo postoperation. Nociceptive reinnervation to the hindpaw was also assessed by plantar algesimetry. Crossed extensor reflexes were evoked by stimulation of the tibial nerve at the ankle and recorded from the contralateral tibialis anterior muscle. Reinnervation of the hindpaw increased progressively with time during the 3 mo after lesion. The degree of muscle and sensory target reinnervation was dependent on the severity of the injury and the nerve gap created. The crossed extensor reflex consisted of three bursts of activity (C1, C2, and C3) of gradually longer latency, lower amplitude, and higher threshold in control rats. During follow-up after sciatic nerve injury, all animals in the operated groups showed recovery of components C1 and C2 and of the reflex H wave, whereas component C3 was detected in a significantly lower proportion of animals in groups with tube repair. The maximal amplitude of components C1 and C2 recovered to values higher than preoperative values, reaching final levels between 150 and 245% at the end of the follow-up in groups CRH, CS, and SIL4. When reflex amplitude was normalized by the CNAP amplitude of the regenerated tibial nerve, components C1 (300–400%) and C2 (150–350%) showed highly increased responses, while C3 was similar to baseline levels. In conclusion, reflexes mediated by myelinated sensory afferents showed, after nerve injuries, a higher degree of facilitation than those mediated by unmyelinated fibers. These changes tended to decline toward baseline values with progressive reinnervation but still remained significant 3 mo after injury.

scholarly journals Effects of Taxol on Regeneration in a Rat Sciatic Nerve Transection Model

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Shih-Tien Hsu ◽  
Chun-Hsu Yao ◽  
Yuan-Man Hsu ◽  
Jia-Horng Lin ◽  
Yung-Hsiang Chen ◽  
...  
Keyword(s):  
Growth Factors ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Nerve Transection ◽  
Cremophor El ◽  
Neuronal Connectivity ◽  
Sciatic Nerve Transection ◽  
Expression Levels ◽  
Nerve Growth Factors

Abstract Recent studies describe taxol as a candidate treatment for promoting central nerve regeneration. However, taxol has serious side effects including peripheral neurotoxicity, and little information is known about the effect of taxol on peripheral nerve regeneration. We investigated the effects of taxol on regeneration in a rat sciatic nerve transection model. Rats were divided into four groups (n = 10): normal saline (i.p.) as the control, Cremophor EL vehicle, and 2 or 6 mg/kg of taxol in the Cremophor EL solution (four times in day-2, 4, 6, and 8), respectively. We evaluated neuronal electrophysiology, animal behaviour, neuronal connectivity, macrophage infiltration, location and expression levels of calcitonin gene-related peptide (CGRP), and expression levels of both nerve growth factors and immunoregulatory factors. In the high-dose taxol group (6 mg/kg), neuronal electrophysiological function was significantly impaired. Licking latencies were significantly changed while motor coordination was unaffected. Neuronal connectivity, macrophage density, and expression levels of CGRP was dramatically reduced. Expression levels of nerve growth factors and immunoregulatory factors was also reduced, while it was increased in the low-dose taxol group (2 mg/kg). These results indicate that taxol can modulate local inflammatory conditions, impair nerve regeneration, and impede recovery of a severe peripheral nerve injury.

scholarly journals Magnetization Transfer Ratio of Peripheral Nerve and Skeletal Muscle

2021 ◽  
Author(s):  
Olivia Fösleitner ◽  
Véronique Schwehr ◽  
Tim Godel ◽  
Fabian Preisner ◽  
Philipp Bäumer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Sciatic Nerve ◽  
Linear Regression ◽  
Peripheral Nerve ◽  
Regression Model ◽  
Multiple Linear Regression ◽  
Linear Regression Model ◽  
Magnetization Transfer ◽  
Multiple Linear Regression Model

Abstract Purpose To assess the correlation of peripheral nerve and skeletal muscle magnetization transfer ratio (MTR) with demographic variables. Methods In this study 59 healthy adults evenly distributed across 6 decades (mean age 50.5 years ±17.1, 29 women) underwent magnetization transfer imaging and high-resolution T2-weighted imaging of the sciatic nerve at 3 T. Mean sciatic nerve MTR as well as MTR of biceps femoris and vastus lateralis muscles were calculated based on manual segmentation on six representative slices. Correlations of MTR with age, body height, body weight, and body mass index (BMI) were expressed by Pearson coefficients. Best predictors for nerve and muscle MTR were determined using a multiple linear regression model with forward variable selection and fivefold cross-validation. Results Sciatic nerve MTR showed significant negative correlations with age (r = −0.47, p < 0.001), BMI (r = −0.44, p < 0.001), and body weight (r = −0.36, p = 0.006) but not with body height (p = 0.55). The multiple linear regression model determined age and BMI as best predictors for nerve MTR (R2 = 0.40). The MTR values were different between nerve and muscle tissue (p < 0.0001), but similar between muscles. Muscle MTR was associated with BMI (r = −0.46, p < 0.001 and r = −0.40, p = 0.002) and body weight (r = −0.36, p = 0.005 and r = −0.28, p = 0.035). The BMI was selected as best predictor for mean muscle MTR in the multiple linear regression model (R2 = 0.26). Conclusion Peripheral nerve MTR decreases with higher age and BMI. Studies that assess peripheral nerve MTR should consider age and BMI effects. Skeletal muscle MTR is primarily associated with BMI but overall less dependent on demographic variables.

scholarly journals SUR1, newly expressed in astrocytes, mediates neuropathic pain in a mouse model of peripheral nerve injury

2021 ◽  
Vol 17 ◽  
pp. 174480692110066
Author(s):  
Orest Tsymbalyuk ◽  
Volodymyr Gerzanich ◽  
Aaida Mumtaz ◽  
Sanketh Andhavarapu ◽  
Svetlana Ivanova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Thermal Sensitivity ◽  
Gradual Improvement ◽  
Pain Behaviors

Background Neuropathic pain following peripheral nerve injury (PNI) is linked to neuroinflammation in the spinal cord marked by astrocyte activation and upregulation of interleukin 6 (IL -6 ), chemokine (C-C motif) ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 1 (CXCL1), with inhibition of each individually being beneficial in pain models. Methods Wild type (WT) mice and mice with global or pGfap-cre- or pGFAP-cre/ERT2-driven Abcc8/SUR1 deletion or global Trpm4 deletion underwent unilateral sciatic nerve cuffing. WT mice received prophylactic (starting on post-operative day [pod]-0) or therapeutic (starting on pod-21) administration of the SUR1 antagonist, glibenclamide (10 µg IP) daily. We measured mechanical and thermal sensitivity using von Frey filaments and an automated Hargreaves method. Spinal cord tissues were evaluated for SUR1-TRPM4, IL-6, CCL2 and CXCL1. Results Sciatic nerve cuffing in WT mice resulted in pain behaviors (mechanical allodynia, thermal hyperalgesia) and newly upregulated SUR1-TRPM4 in dorsal horn astrocytes. Global and pGfap-cre-driven Abcc8 deletion and global Trpm4 deletion prevented development of pain behaviors. In mice with Abcc8 deletion regulated by pGFAP-cre/ERT2, after pain behaviors were established, delayed silencing of Abcc8 by tamoxifen resulted in gradual improvement over the next 14 days. After PNI, leakage of the blood-spinal barrier allowed entry of glibenclamide into the affected dorsal horn. Daily repeated administration of glibenclamide, both prophylactically and after allodynia was established, prevented or reduced allodynia. The salutary effects of glibenclamide on pain behaviors correlated with reduced expression of IL-6, CCL2 and CXCL1 by dorsal horn astrocytes. Conclusion SUR1-TRPM4 may represent a novel non-addicting target for neuropathic pain.

scholarly journals IL-17F depletion accelerates chitosan conduit guided peripheral nerve regeneration

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Feixiang Chen ◽  
Weihuang Liu ◽  
Qiang Zhang ◽  
Ping Wu ◽  
Ao Xiao ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Knockout Mice ◽  
Inflammatory Markers ◽  
Nerve Repair ◽  
Peripheral Nerve Regeneration ◽  
Wild Type ◽  
Anti Inflammatory

AbstractPeripheral nerve injury is a serious health problem and repairing long nerve deficits remains a clinical challenge nowadays. Nerve guidance conduit (NGC) serves as the most promising alternative therapy strategy to autografts but its repairing efficiency needs improvement. In this study, we investigated whether modulating the immune microenvironment by Interleukin-17F (IL-17F) could promote NGC mediated peripheral nerve repair. Chitosan conduits were used to bridge sciatic nerve defect in IL-17F knockout mice and wild-type mice with autografts as controls. Our data revealed that IL-17F knockout mice had improved functional recovery and axonal regeneration of sciatic nerve bridged by chitosan conduits comparing to the wild-type mice. Notably, IL-17F knockout mice had enhanced anti-inflammatory macrophages in the NGC repairing microenvironment. In vitro data revealed that IL-17F knockout peritoneal and bone marrow derived macrophages had increased anti-inflammatory markers after treatment with the extracts from chitosan conduits, while higher pro-inflammatory markers were detected in the Raw264.7 macrophage cell line, wild-type peritoneal and bone marrow derived macrophages after the same treatment. The biased anti-inflammatory phenotype of macrophages by IL-17F knockout probably contributed to the improved chitosan conduit guided sciatic nerve regeneration. Additionally, IL-17F could enhance pro-inflammatory factors production in Raw264.7 cells and wild-type peritoneal macrophages. Altogether, IL-17F may partially mediate chitosan conduit induced pro-inflammatory polarization of macrophages during nerve repair. These results not only revealed a role of IL-17F in macrophage function, but also provided a unique and promising target, IL-17F, to modulate the microenvironment and enhance the peripheral nerve regeneration.

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