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  • 1
    Online Resource
    Online Resource
    Brain-Derived Neurotrophic Factor Is Released in the Dorsal Horn by Distinctive Patterns of Afferent Fiber Stimulation
    Society for Neuroscience ; 2001
    In:  The Journal of Neuroscience Vol. 21, No. 12 ( 2001-06-15), p. 4469-4477
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 21, No. 12 ( 2001-06-15), p. 4469-4477
    Abstract: Brain-derived neurotrophic factor (BDNF) is synthesized by small neuron cell bodies in the dorsal root ganglia (DRG) and is anterogradely transported to primary afferent terminals in the dorsal horn where it is involved in the modulation of painful stimuli. Here we show that BDNF is released in the rat isolated dorsal horn after chemical stimulation by capsaicin or electrical stimulation of dorsal roots. Capsaicin superfusion (1–100 μ m ) induced a dose-dependent release of BDNF, measured using ELISA. The highest dose of capsaicin also induced a depletion of BDNF protein in the dorsal horn. BDNF release was also seen after electrical stimulation of the dorsal roots at C-fiber strength. This release was encoded by specific patterns of afferent fiber stimulation. Neither continuous low-frequency (480 pulses, 1 Hz) nor tetanic high-frequency (300 pulses in 3 trains, 100 Hz) stimulation evoked release of BDNF, although substance P (SP) release was observed under both of these conditions. However, BDNF was released after short bursts of high-frequency stimulation (300 pulses in 75 trains, 100 Hz) along with SP and glutamate. The NMDA antagonist d -AP-5 inhibited electrically evoked BDNF release. BDNF release was also measured after systemic or intrathecal NGF treatment. This upregulated BDNF content in the DRG and increased the capsaicin-evoked release of BDNF. Similarly, the amount of BDNF released by burst stimulation was increased after NGF treatment. This activity-dependent release continued to be encoded solely by this stimulation pattern. These experiments demonstrate that BDNF release in the dorsal horn is encoded by specific patterns of afferent fiber stimulation and is mediated by NMDA receptor activation.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.21-12-04469.2001
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2001
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Development and comparison of biosensors for in-vivo applications
    Royal Society of Chemistry (RSC) ; 2000
    In:  Faraday Discussions Vol. 116 ( 2000), p. 291-303
    Details
    In: Faraday Discussions, Royal Society of Chemistry (RSC), Vol. 116 ( 2000), p. 291-303
    Type of Medium: Online Resource
    ISSN: 1359-6640 , 1364-5498
    URL: Article
    DOI: 10.1039/b003256p
    Language: Unknown
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2000
    detail.hit.zdb_id: 1472891-6
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  • 3
    Online Resource
    Online Resource
    Small Water Bodies in Great Britain and Ireland: Ecosystem function, human-generated degradation, and options for restorative action
    Elsevier BV ; 2018
    In:  Science of The Total Environment Vol. 645 ( 2018-12), p. 1598-1616
    Details
    In: Science of The Total Environment, Elsevier BV, Vol. 645 ( 2018-12), p. 1598-1616
    Type of Medium: Online Resource
    ISSN: 0048-9697
    URL: Article
    DOI: 10.1016/j.scitotenv.2018.07.243
    RVK:
    AR 10100
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 1498726-0
    detail.hit.zdb_id: 121506-1
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Effect of Work: Rest Ratio on Cycling Performance Following Sprint Interval Training: A Randomized Control Trial
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Journal of Strength and Conditioning Research Vol. 33, No. 12 ( 2019-12), p. 3263-3268
    Details
    In: Journal of Strength and Conditioning Research, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 12 ( 2019-12), p. 3263-3268
    Abstract: Lloyd Jones, MC, Morris, MG, and Jakeman, JR. Effect of work: Rest ratio on cycling performance following sprint interval training: A randomized control trial. J Strength Cond Res 33(12): 3263–3268, 2019—Sprint interval training (SIT) has been shown to improve performance measures in a range of individuals, and it is understood that different responses can be elicited from different training protocols. However, consideration of changes in work to rest ratios could offer important insight into optimizing training programs. The purpose of this study was to investigate the effect of 3 different work to rest ratios on exercise performance. Thirty-six male and female subjects were randomly allocated to 1 of 3 training groups or a nontraining control group. Training consisted of 10 × 6 second “all-out” sprints on a cycle ergometer, with a 1:8, 1:10, or 1:12 work-to-rest ratio. Performance data, including peak power output, performance decrement, and 10-km time trial performance data were collected before and after 2 weeks of SIT. There were significant ( p ≤ 0.05) improvements in all parameters for the training groups, but no changes were observed in the control condition. Peak power increased by 57.2, 50.7, and 53.7 W in the 1:8, 1:10 and 1:12 groups, respectively, with no significant differences in response between conditions. Time trial performance improved significantly in all 3 training conditions (29.4, 8.7, and 25.1 seconds in the 1:8, 1:10, and 1:12 groups), while worsening in the control group. All training conditions resulted in significant improvements in performance, but there were no significant differences in improvement for any of the groups. Any of the 3 stated that work to rest ratios would be appropriate for use with athletes and allow some level of personal preference for those interested in using the protocol.
    Type of Medium: Online Resource
    ISSN: 1064-8011
    URL: Article
    DOI: 10.1519/JSC.0000000000003381
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2142889-X
    SSG: 31
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  • 5
    Online Resource
    Online Resource
    Dynamic Changes in Brain Glucose and Lactate in Pericontusional Areas of the Human Cerebral Cortex, Monitored with Rapid Sampling On-Line Microdialysis: Relationship with Depolarisation-Like Events
    SAGE Publications ; 2005
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 25, No. 3 ( 2005-03), p. 402-413
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 25, No. 3 ( 2005-03), p. 402-413
    Abstract: The pathophysiology of peri-lesion boundary zones in acute brain injury is highly dynamic, and it is now clear that spreading-depression-like events occur frequently in areas of cerebral cortex adjacent to contusions in the injured human brain. An automated method to assay microdialysate from peri-lesion cerebral cortex in 11 patients with intracranial haematomas requiring surgery was used. Perfusate (2 μL/min) flowed directly into a flow-injection system for assay of glucose and lactate at intervals typically of 30 secs each. Four channels of electrocorticogram (ECoG) were recorded from a subdural strip adjacent to the catheter. Several patterns of change in metabolites were identified in different time domains. Overall, the number of transient lactate events was significantly correlated with the number of glucose events ( r 2 =0.48, P=0.027, n=10). Progressive reduction in dialysate glucose was very closely correlated with the aggregate number of ECoG events ( r 2 =0.76, P=0.0004, n=11). It is proposed that the recently documented adverse impact of low dialysate glucose on clinical outcome may be because of recurrent, spontaneous spreading-depression-like events in the perilesion cortex.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/sj.jcbfm.9600051
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2005
    detail.hit.zdb_id: 2039456-1
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  • 6
    Online Resource
    Online Resource
    Neuromodulation using ultra low frequency current waveform reversibly blocks axonal conduction and chronic pain
    American Association for the Advancement of Science (AAAS) ; 2021
    In:  Science Translational Medicine Vol. 13, No. 608 ( 2021-08-25)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 13, No. 608 ( 2021-08-25)
    Abstract: Chronic pain remains a leading cause of disability worldwide, and there is still a clinical reliance on opioids despite the medical side effects associated with their use and societal impacts associated with their abuse. An alternative approach is the use of electrical neuromodulation to produce analgesia. Direct current can block action potential propagation but leads to tissue damage if maintained. We have developed a form of ultra low frequency (ULF) biphasic current and studied its effects. In anesthetized rats, this waveform produced a rapidly developing and completely reversible conduction block in 〉 85% of spinal sensory nerve fibers excited by peripheral stimulation. Sustained ULF currents at lower amplitudes led to a slower onset but reversible conduction block. Similar changes were seen in an animal model of neuropathic pain, where ULF waveforms blocked sensory neuron ectopic activity, known to be an important driver of clinical neuropathic pain. Using a computational model, we showed that prolonged ULF currents could induce accumulation of extracellular potassium, accounting for the slowly developing block observed in rats. Last, we tested the analgesic effects of epidural ULF currents in 20 subjects with chronic leg and back pain. Pain ratings improved by 90% after 2 weeks. One week after explanting the electrodes, pain ratings reverted to 72% of pretreatment screening value. We conclude that epidural spinal ULF neuromodulation represents a promising therapy for treating chronic pain.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.abg9890
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2021
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  • 7
    Online Resource
    Online Resource
    Stereoselective Effects of 2,3-benzodiazepines In Vivo : Electrophysiology and Neuroprotection Studies
    Elsevier BV ; 1996
    In:  Neuropharmacology Vol. 35, No. 12 ( 1996-12), p. 1681-1688
    Details
    In: Neuropharmacology, Elsevier BV, Vol. 35, No. 12 ( 1996-12), p. 1681-1688
    Type of Medium: Online Resource
    ISSN: 0028-3908
    URL: Article
    DOI: 10.1016/S0028-3908(96)00155-4
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1996
    detail.hit.zdb_id: 1500655-4
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  • 8
    Online Resource
    Online Resource
    Reduced adenosine uptake accelerates ischaemic block of population spikes in hippocampal slices from streptozotocin‐treated diabetic rats
    Wiley ; 1998
    In:  European Journal of Neuroscience Vol. 10, No. 1 ( 1998-01), p. 239-245
    Details
    In: European Journal of Neuroscience, Wiley, Vol. 10, No. 1 ( 1998-01), p. 239-245
    Abstract: We have used rats with streptozotocin‐induced diabetes to investigate the effects of hyperglycaemia‐mediated impaired nucleoside uptake on the actions of endogenous adenosine in hippocampal slices. In control tissue under conditions of anoxia and aglycaemia the rise in the extracellular adenosine concentration resulted in complete inhibition of synaptic activity in about 2 min. In slices from previously hyperglycaemic rats the inhibition of synaptically mediated responses occurred significantly faster, although this change could be prevented by insulin treatment. Application of the selective adenosine A1 receptor antagonist [8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX)] prevented the anoxia/aglycaemia‐mediated inhibition and, furthermore, abolished the differences in the electrophysiological responses between control and diabetic tissue. The effects of impaired nucleoside uptake could be mimicked in control slices by applying the nucleoside uptake blocker hydroxynitrobenzylthioinosine (HNBTI). This had the effect of speeding up the rate of anoxia/aglycaemia‐induced synaptic inhibition in control tissue to that seen in diabetic tissue. However, such treatment had no effect on the responses in diabetic tissue as expected if the HNBTI‐sensitive uptake process was already inhibited by the chronic hyperglycaemia. The impairment of nucleoside uptake by chronic hyperglycaemia results in the potentiation of the modulatory actions of endogenous adenosine in the central nervous system. Such an alteration in adenosine function may be important in explaining behavioural and pathological changes associated with diabetes mellitus.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Article
    DOI: 10.1046/j.1460-9568.1998.00035.x
    Language: English
    Publisher: Wiley
    Publication Date: 1998
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Abnormal substance P release from the spinal cord following injury to primary sensory neurons
    Wiley ; 2000
    In:  European Journal of Neuroscience Vol. 12, No. 1 ( 2000-01), p. 397-399
    Details
    In: European Journal of Neuroscience, Wiley, Vol. 12, No. 1 ( 2000-01), p. 397-399
    Abstract: The neuropeptide substance P (SP) modulates nociceptive transmission within the spinal cord. Normally, SP is uniquely contained in a subpopulation of small‐calibre axons (Aδ‐ and C‐fibres) within primary afferent nerve. However, it has been shown that after nerve transection, besides being downregulated in small axons, SP is expressed de novo in large myelinated Aβ‐fibres. In this study we investigated whether, following peripheral nerve injury, SP was released de novo from the spinal cord after selective activation of Aβ‐fibres. Spinal cords with dorsal roots attached were isolated in vitro from rats 2 weeks following distal sciatic axotomy or proximal spinal nerve lesion (SNL). The ipsilateral dorsal roots were electrically stimulated for two consecutive periods at low‐ or high‐threshold fibre strength, spinal cord superfusates were collected and SP content was determined by radioimmunoassay. SNL, but not axotomized or control rat cords, released significant amounts of SP after selective activation of Aβ‐fibres. Not only do these data support the idea that Aβ myelinated fibres contribute to neuropathic pain by releasing SP, they also illustrate the importance of the proximity of the lesion to the cell body.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Article
    DOI: 10.1046/j.1460-9568.2000.00946.x
    Language: English
    Publisher: Wiley
    Publication Date: 2000
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Spreading and Synchronous Depressions of Cortical Activity in Acutely Injured Human Brain
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Stroke Vol. 33, No. 12 ( 2002-12), p. 2738-2743
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 12 ( 2002-12), p. 2738-2743
    Abstract: Background and Purpose— Cortical spreading depression (CSD) has been much studied experimentally but never demonstrated unequivocally in human neocortex by direct electrophysiological recording. A similar phenomenon, peri-infarct depolarization, occurs in experimental models of stroke and causes the infarct to enlarge. Our current understanding of the mechanisms of deterioration in the days after major traumatic or ischemic brain injury in humans has not yielded any effective, novel drug treatment. This study sought clear evidence for the occurrence and propagation of CSD in the injured human brain. Methods— In 14 patients undergoing neurosurgery after head injury or intracranial hemorrhage, we placed electrocorticographic (ECoG) electrodes near foci of damaged cortical tissue. Results— Transient episodes of depressed ECoG activity that propagated across the cortex at rates in the range of 0.6 to 5.0 mm/min were observed in 5 patients; this rate of propagation is characteristic of CSD. We also observed, in 8 of the 14 patients, transient depressions of ECoG amplitude that appeared essentially simultaneous in all recording channels, without clear evidence of spread. Conclusions— These results indicate that CSD or similar events occur in the injured human brain and are more frequent than previously suggested. On the basis of these observations, we suggest that the related phenomenon, peri-infarct depolarization, is indeed likely to occur in boundary zones in the ischemic human cerebral cortex.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.0000043073.69602.09
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 1467823-8
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