Database : MEDLINE
Search on : Neural and Conduction [Words]
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[PMID]: 29408605
[Au] Autor:Truong K; Ahmad I; Jason Clark J; Seline A; Bertroche T; Mostaert B; Van Daele DJ; Hansen MR
[Ad] Address:Department of Otolaryngology-Head and Neck Surgery, University of Iowa, Iowa City, IA 52242, United States.
[Ti] Title:Nf2 Mutation in Schwann Cells Delays Functional Neural Recovery Following Injury.
[So] Source:Neuroscience;374:205-213, 2018 Mar 15.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Merlin is the protein product of the NF2 tumor suppressor gene. Germline NF2 mutation leads to neurofibromatosis type 2 (NF2), characterized by multiple intracranial and spinal schwannomas. Patients with NF2 also frequently develop peripheral neuropathies. While the role of merlin in SC neoplasia is well established, its role in SC homeostasis is less defined. Here we explore the role of merlin in SC responses to nerve injury and their ability to support axon regeneration. We performed sciatic nerve crush in wild-type (WT) and in P0SchΔ39-121 transgenic mice that express a dominant negative Nf2 isoform in SCs. Recovery of nerve function was assessed by measuring mean contact paw area on a pressure pad 7, 21, 60, and 90 days following nerve injury and by nerve conduction assays at 90 days following injury. After 90 days, the nerves were harvested and axon regeneration was quantified stereologically. Myelin ultrastructure was analyzed by electron microscopy. Functional studies showed delayed nerve regeneration in Nf2 mutant mice compared to the WT mice. Delayed neural recovery correlated with a reduced density of regenerated axons and increased endoneurial space in mutants compared to WT mice. Nevertheless, functional and nerve conduction measures ultimately recovered to similar levels in WT and Nf2 mutant mice, while there was a small (∼17%) reduction in the percent of regenerated axons in the Nf2 mutant mice. The data suggest that merlin function in SCs regulates neural ultrastructure and facilitates neural regeneration, in addition to its role in SC neoplasia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

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[PMID]: 29370962
[Au] Autor:Skoe E; Tufts J
[Ad] Address:Department of Speech, Language, and Hearing Sciences, University of Connecticut, Storrs, CT, 06269, USA; Department of Psychological Sciences, Cognitive Sciences Program, University of Connecticut, Storrs, CT, 06269, USA; Connecticut Institute for Brain and Cognitive Sciences, University of Connecticut, Storrs, CT, 06269, USA. Electronic address: erika.skoe@uconn.edu.
[Ti] Title:Evidence of noise-induced subclinical hearing loss using auditory brainstem responses and objective measures of noise exposure in humans.
[So] Source:Hear Res;361:80-91, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Exposure to loud sound places the auditory system at considerable risk, especially when the exposure is routine. The current study examined the impact of routine auditory overexposure in young human adults with clinically-normal audiometric thresholds by measuring the auditory brainstem response (ABR), an electrophysiological measure of peripheral and central auditory processing. Sound exposure was measured objectively with body-worn noise dosimeters over a week. Participants were divided into low-exposure and high-exposure groups, with the low-exposure group having an average daily noise exposure dose of ∼11% of the recommended exposure limit compared to the high-exposure group average of nearly 500%. Compared to the low-exposure group, the high-exposure group had delayed ABRs to suprathreshold click stimuli and this prolongation was evident at ABR waves I and III but strongest for V. When peripheral differences were corrected using the I-V interpeak latency, the high-exposure group showed greater taxation at faster stimulus presentation rates than the low-exposure group, suggestive of neural conduction inefficiencies within central auditory structures. Our findings are consistent with the hypothesis that auditory overexposure affects peripheral and central auditory structures even before changes are evident on standard audiometry. We discuss our findings within the context of the larger debate on the mechanisms and manifestations of subclinical hearing loss.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  3 / 34689 MEDLINE  
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[PMID]: 29474352
[Au] Autor:Abeysuriya RG; Hadida J; Sotiropoulos SN; Jbabdi S; Becker R; Hunt BAE; Brookes MJ; Woolrich MW
[Ad] Address:Oxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, United Kingdom.
[Ti] Title:A biophysical model of dynamic balancing of excitation and inhibition in fast oscillatory large-scale networks.
[So] Source:PLoS Comput Biol;14(2):e1006007, 2018 Feb.
[Is] ISSN:1553-7358
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Over long timescales, neuronal dynamics can be robust to quite large perturbations, such as changes in white matter connectivity and grey matter structure through processes including learning, aging, development and certain disease processes. One possible explanation is that robust dynamics are facilitated by homeostatic mechanisms that can dynamically rebalance brain networks. In this study, we simulate a cortical brain network using the Wilson-Cowan neural mass model with conduction delays and noise, and use inhibitory synaptic plasticity (ISP) to dynamically achieve a spatially local balance between excitation and inhibition. Using MEG data from 55 subjects we find that ISP enables us to simultaneously achieve high correlation with multiple measures of functional connectivity, including amplitude envelope correlation and phase locking. Further, we find that ISP successfully achieves local E/I balance, and can consistently predict the functional connectivity computed from real MEG data, for a much wider range of model parameters than is possible with a model without ISP.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pcbi.1006007

  4 / 34689 MEDLINE  
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[PMID]: 29480857
[Au] Autor:Shi M; Qi H; Ding H; Chen F; Xin Z; Zhao Q; Guan S; Shi H
[Ad] Address:Department of Ultrasound, Qianfoshan Hospital Affiliated to Shandong University, Jinan.
[Ti] Title:Electrophysiological examination and high frequency ultrasonography for diagnosis of radial nerve torsion and compression.
[So] Source:Medicine (Baltimore);97(2):e9587, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This study aims to evaluate the value of electrophysiological examination and high frequency ultrasonography in the differential diagnosis of radial nerve torsion and radial nerve compression.Patients with radial nerve torsion (n = 14) and radial nerve compression (n = 14) were enrolled. The results of neurophysiological and high frequency ultrasonography were compared.Electrophysiological examination and high-frequency ultrasonography had a high diagnostic rate for both diseases with consistent results. Of the 28 patients, 23 were positive for electrophysiological examination, showing decreased amplitude and decreased conduction velocity of radial nerve; however, electrophysiological examination cannot distinguish torsion from compression. A total of 27 cases showed positive in ultrasound examinations among all 28 cases. On ultrasound images, the nerve was thinned at torsion site whereas thickened at the distal ends of torsion. The diameter and cross-sectional area of torsion or compression determined the nerve damage, and ultrasound could locate the nerve injury site and measure the length of the nerve.Electrophysiological examination and high-frequency ultrasonography can diagnose radial neuropathy, with electrophysiological examination reflecting the neurological function, and high-frequency ultrasound differentiating nerve torsion from compression.
[Mh] MeSH terms primary: Electrodiagnosis
Nerve Compression Syndromes/diagnosis
Radial Nerve/diagnostic imaging
Radial Nerve/physiopathology
Radial Neuropathy/diagnosis
Ultrasonography
[Mh] MeSH terms secundary: Adolescent
Adult
Diagnosis, Differential
Female
Humans
Male
Nerve Compression Syndromes/physiopathology
Nerve Compression Syndromes/surgery
Neural Conduction
Radial Nerve/surgery
Radial Neuropathy/physiopathology
Radial Neuropathy/surgery
Treatment Outcome
Young Adult
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009587

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[PMID]: 28743796
[Au] Autor:Roberts SL; Dun XP; Doddrell RDS; Mindos T; Drake LK; Onaitis MW; Florio F; Quattrini A; Lloyd AC; D'Antonio M; Parkinson DB
[Ad] Address:Plymouth University Peninsula Schools of Medicine and Dentistry, John Bull Building, Plymouth Science Park, Plymouth PL6 8BU, UK.
[Ti] Title:Sox2 expression in Schwann cells inhibits myelination and induces influx of macrophages to the nerve.
[So] Source:Development;144(17):3114-3125, 2017 09 01.
[Is] ISSN:1477-9129
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Correct myelination is crucial for the function of the peripheral nervous system. Both positive and negative regulators within the axon and Schwann cell function to ensure the correct onset and progression of myelination during both development and following peripheral nerve injury and repair. The Sox2 transcription factor is well known for its roles in the development and maintenance of progenitor and stem cell populations, but has also been proposed as a negative regulator of myelination in Schwann cells. We wished to test fully whether Sox2 regulates myelination and show here that, in mice, sustained Sox2 expression blocks myelination in the peripheral nerves and maintains Schwann cells in a proliferative non-differentiated state, which is also associated with increased inflammation within the nerve. The plasticity of Schwann cells allows them to re-myelinate regenerated axons following injury and we show that re-myelination is also blocked by Sox2 expression in Schwann cells. These findings identify Sox2 as a physiological regulator of Schwann cell myelination and its potential to play a role in disorders of myelination in the peripheral nervous system.
[Mh] MeSH terms primary: Macrophages/metabolism
Myelin Sheath/metabolism
Peripheral Nerves/metabolism
SOXB1 Transcription Factors/metabolism
Schwann Cells/metabolism
[Mh] MeSH terms secundary: Animals
Biomarkers/metabolism
Cadherins/metabolism
Cell Proliferation
Early Growth Response Protein 2/metabolism
Green Fluorescent Proteins/metabolism
Mice, Transgenic
Motor Activity
Neural Conduction
Peripheral Nerve Injuries/metabolism
Peripheral Nerve Injuries/pathology
Peripheral Nerves/pathology
Peripheral Nerves/ultrastructure
Proto-Oncogene Proteins c-jun/metabolism
Rats
Recovery of Function
Schwann Cells/pathology
Transgenes
beta Catenin/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Biomarkers); 0 (Cadherins); 0 (Early Growth Response Protein 2); 0 (Proto-Oncogene Proteins c-jun); 0 (SOXB1 Transcription Factors); 0 (beta Catenin); 147336-22-9 (Green Fluorescent Proteins)
[Em] Entry month:1710
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[Js] Journal subset:IM
[Da] Date of entry for processing:170727
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150656

  6 / 34689 MEDLINE  
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[PMID]: 29425906
[Au] Autor:Pelot NA; Grill WM
[Ad] Address:Department of Biomedical Engineering, Duke University, Room 1427, Fitzpatrick CIEMAS, 101 Science Drive, Campus Box 90281, Durham, NC, USA.
[Ti] Title:Effects of vagal neuromodulation on feeding behavior.
[So] Source:Brain Res;, 2018 Feb 07.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Implanted vagus nerve stimulation (VNS) for obesity was recently approved by the FDA. However, its efficacy and mechanisms of action remain unclear. Herein, we synthesize clinical and preclinical effects of VNS on feeding behavior and energy balance and discuss engineering considerations for understanding and improving the therapy. Clinical cervical VNS (≤30 Hz) to treat epilepsy or depression has produced mixed effects on weight loss as a side effect, albeit in uncontrolled, retrospective studies. Conversely, preclinical studies (cervical and subdiaphragmatic VNS) mostly report decreased food intake and either decreased weight gain or weight loss. More recent clinical studies report weight loss in response to kilohertz frequency VNS applied to the subdiaphragmatic vagi, albeit with a large placebo effect. Rather than eliciting neural activity, this therapy putatively blocks conduction in the vagus nerves. Overall, stimulation parameters lack systematic exploration, optimization, and justification based on target nerve fibers and therapeutic outcomes. The vagus nerve transduces, transmits, and integrates important neural (efferent and afferent), humoral, energetic, and inflammatory information between the gut and brain. Thus, improved understanding of the biophysics, electrophysiology, and (patho)physiology has the potential to advance VNS as an effective therapy for a wide range of diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher

  7 / 34689 MEDLINE  
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[PMID]: 29225064
[Au] Autor:Mikulan E; Hesse E; Sedeo L; Bekinschtein T; Sigman M; Garca MDC; Silva W; Ciraolo C; Garca AM; Ibez A
[Ad] Address:Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCYT), INECO Foundation, Favaloro University, Buenos Aires, Argentina; National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina; Consciousness and Cogni
[Ti] Title:Intracranial high-γ connectivity distinguishes wakefulness from sleep.
[So] Source:Neuroimage;169:265-277, 2017 Dec 08.
[Is] ISSN:1095-9572
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Neural synchrony in the γ-band is considered a fundamental process in cortical computation and communication and it has also been proposed as a crucial correlate of consciousness. However, the latter claim remains inconclusive, mainly due to methodological limitations, such as the spectral constraints of scalp-level electroencephalographic recordings or volume-conduction confounds. Here, we circumvented these caveats by comparing γ-band connectivity between two global states of consciousness via intracranial electroencephalography (iEEG), which provides the most reliable measurements of high-frequency activity in the human brain. Non-REM Sleep recordings were compared to passive-wakefulness recordings of the same duration in three subjects with surgically implanted electrodes. Signals were analyzed through the weighted Phase Lag Index connectivity measure and relevant graph theory metrics. We found that connectivity in the high-γ range (90-120Hz), as well as relevant graph theory properties, were higher during wakefulness than during sleep and discriminated between conditions better than any other canonical frequency band. Our results constitute the first report of iEEG differences between wakefulness and sleep in the high-γ range at both local and distant sites, highlighting the utility of this technique in the search for the neural correlates of global states of consciousness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:Publisher

  8 / 34689 MEDLINE  
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[PMID]: 29477243
[Au] Autor:Parry LV; Maslin MRD; Schaette R; Moore DR; Munro KJ
[Ad] Address:Manchester Centre for Audiology and Deafness, School of Health Sciences, University of Manchester, Oxford Road, Manchester, M13 9PL, United Kingdom. Electronic address: lauren.parry@mcht.nhs.uk.
[Ti] Title:Increased auditory cortex neural response amplitude in adults with chronic unilateral conductive hearing impairment.
[So] Source:Hear Res;, 2018 Feb 02.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Animal studies have demonstrated that unilateral hearing loss can induce changes in neural response amplitude of the mature central auditory system (CAS). However, there is limited physiological evidence of these neural gain changes in the auditory cortex of human adults. The present study investigated the impact of chronic, unilateral conductive hearing impairment on cortical auditory evoked potentials (CAEPs) recorded from 15 adults (21-65 years old) in response to a 1 kHz tone (80 ms duration) presented to the impaired ear via a bone conduction transducer. The amplitude and latency of the main CAEP components were compared to those obtained from normal hearing age-matched control participants. Both P1-N1 and N1-P2 amplitudes were significantly larger in the hearing impaired relative to the control participants. Differences between groups in the mean latencies of P1, N1, and P2 were not statistically significant. These results are the first to provide direct evidence of increased neural response amplitude in the adult human auditory cortex in the presence of unilateral conductive hearing loss. Importantly, the study shows that central gain changes are a direct result of deprivation of sound rather than cochlear or neural pathology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[St] Status:Publisher

  9 / 34689 MEDLINE  
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[PMID]: 29412513
[Au] Autor:Coppey LJ; Shevalye H; Obrosov A; Davidson EP
[Ad] Address:Department of Internal Medicine, The University of Iowa, Iowa City, IA, 52242.
[Ti] Title:Determination of peripheral neuropathy in high fat fed low dose streptozotocin treated female C57Bl/6J mice and Sprague-Dawley rats.
[So] Source:J Diabetes Investig;, 2018 Feb 07.
[Is] ISSN:2040-1124
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:AIMS/INTRODUCTION: Peripheral neuropathy is a common complication of diabetes and also occurs in 30% of human obese subjects with impaired glucose tolerance. Even though peripheral neuropathy affects both genders most pre-clinical studies have been performed using male rodents. The aim of this study was to create diet induced obesity and type 2 diabetes in female rats and mice in order to examine development of peripheral neuropathy. MATERIALS AND METHODS: At twelve weeks of age rats and mice were separated into three groups. Two groups or rats and mice were fed a 60 kcal% high fat diet for 12 weeks (rats) or 8 weeks (mice). To induce type 2 diabetes, one group of high fat fed rats and mice were treated with a low dose of streptozotocin. Analyses of multiple neural endpoints were performed 12 weeks later. RESULTS: Glucose utilization was impaired in diet-induced obese female rats and mice as was a number of neurological endpoints including nerve conduction velocity, intraepidermal and sub-epithelial corneal nerve fiber densities, and thermal and mechanical sensitivity. When female diet-induced obese rats or mice were made hyperglycemic glucose utilization and sensory nerve density of the skin and cornea as well as thermal and mechanical sensitivity were more significantly impaired compared to diet induced obese female rodents. CONCLUSIONS: These studies demonstrate that diet-induced obese and type 2 diabetic female rodents develop peripheral neuropathy that is similar to that occurs in male rodents. However, for female rats more aggressive treatment is required to induce dietary obesity. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:Publisher
[do] DOI:10.1111/jdi.12814

  10 / 34689 MEDLINE  
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[PMID]: 29185418
[Au] Autor:McArdle F
[Ti] Title:Making Local Anesthesia Delivery More Comfortable.
[So] Source:Dent Today;35(11):35, 36-8, 2016 Nov.
[Is] ISSN:8750-2186
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Anesthesia, Dental/methods
Anesthesia, Local
Anesthetics, Local/administration & dosage
[Mh] MeSH terms secundary: Humans
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anesthetics, Local)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:D
[Da] Date of entry for processing:171201
[St] Status:MEDLINE


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