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1.
Background: Acute exercise can increase motor cortical excitability and enhance motor learning in healthy individuals, an effect known as exercise priming. Whether it has the same effects in people with stroke is unclear.

Objectives: The objective of this study was to investigate whether a short, clinically-feasible high-intensity exercise protocol can increase motor cortical excitability in non-exercised muscles of chronic stroke survivors.

Methods: Thirteen participants with chronic, unilateral stroke participated in two sessions, at least one week apart, in a crossover design. In each session, they underwent either high-intensity lower extremity exercise or quiet rest. Motor cortical excitability of the extensor carpi radialis muscles was measured bilaterally with transcranial magnetic stimulation before and immediately after either exercise or rest. Motor cortical excitability changes (post-exercise or rest measures normalized to pre-test measures) were compared between exercise vs. rest conditions.

Results: All participants were able to reach the target high-intensity exercise level. Blood lactate levels increased significantly after exercise (p < .001, d = 2.85). Resting motor evoked potentials from the lesioned hemisphere increased after exercise (mean 1.66; 95% CI: 1.19, 2.13) compared to the rest condition (mean 1.23; 95% CI: 0.64, 1.82), p = .046, d = 2.76, but this was not the case for the non-lesioned hemisphere (p = .406, d = 0.25).

Conclusions: High-intensity exercise can increase lesioned hemisphere motor cortical excitability in a non-exercised muscle post-stroke. Our short and clinically-advantageous exercise protocol shows promise as a potential priming method in stroke rehabilitation.  相似文献   

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Current noninvasive methods to detect structural plasticity in humans are mainly used to study long‐term changes. Diffusion magnetic resonance imaging (MRI) was recently proposed as a novel approach to reveal gray matter changes following spatial navigation learning and object‐location memory tasks. In the present work, we used diffusion MRI to investigate the short‐term neuroplasticity that accompanies motor sequence learning. Following a 45‐min training session in which participants learned to accurately play a short sequence on a piano keyboard, changes in diffusion properties were revealed mainly in motor system regions such as the premotor cortex and cerebellum. In a second learning session taking place immediately afterward, feedback was given on the timing of key pressing instead of accuracy, while participants continued to learn. This second session induced a different plasticity pattern, demonstrating the dynamic nature of learning‐induced plasticity, formerly thought to require months of training in order to be detectable. These results provide us with an important reminder that the brain is an extremely dynamic structure. Furthermore, diffusion MRI offers a novel measure to follow tissue plasticity particularly over short timescales, allowing new insights into the dynamics of structural brain plasticity.  相似文献   
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Background: Anomia, difficulty producing words, is a pervasive symptom of many individuals with aphasia. We have developed a treatment for naming deficits—the Phonological Components Analysis (PCA) protocol—that has proven efficacious in improving word-finding abilities for individuals with post-stroke aphasia.

Aims: The aim of this investigation is to present preliminary findings exploring the potential influence of choice—that is the active engagement of a participant in therapy—on our PCA treatment.

Methods & Procedures: Five individuals with aphasia were treated in one of two conditions—Choice or No Choice. Potential changes in neural activation as a function of the treatment were also investigated. Two individuals (one from each condition) underwent functional MRI (fMRI) pre- and post-therapy.

Outcomes & Results: All the individuals demonstrated a significant treatment effect immediately post-treatment and at a 4-week follow-up and four of the five participants at an 8-week follow-up. Three also demonstrated generalisation to untrained items. Unfortunately, no clear-cut patterns emerged to allow us to make claims about the influence of choice, per se, on the behavioural manifestations of improved naming. Interestingly, the participant from the Choice condition showed neural activation changes post-treatment in frontal and parietal regions that were not evident for the participant in the No Choice condition. Moreover, these changes were accompanied by a larger treatment effect for that individual and generalisation to a novel naming task.

Conclusion: The efficacy of PCA treatment for naming deficits is further supported. In addition, the neuroimaging data suggest the possibility that active engagement of an individual in his/her therapy (in this case choosing phonological attributes of a target word) may exercise executive functions important for success in treating anomia. Also, continued exploration of task factors that may promote even better treatment effects using this protocol is warranted, as is continued investigation of the neural underpinnings associated with treatment effects.  相似文献   
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Tooth loss is common, and exploring the neuroplastic capacity of the face primary motor cortex (face‐M1) and adjacent primary somatosensory cortex (face‐S1) is crucial for understanding how subjects adapt to tooth loss and their prosthetic replacement. The aim was to test if functional reorganization of jaw and tongue motor representations in the rat face‐M1 and face‐S1 occurs following tooth extraction, and if subsequent dental implant placement can reverse this neuroplasticity. Rats (n = 22) had the right maxillary molar teeth extracted under local and general anesthesia. One month later, seven rats had dental implant placement into healed extraction sites. Naive rats (n = 8) received no surgical treatment. Intracortical microstimulation (ICMS) and recording of evoked jaw and tongue electromyographic responses were used to define jaw and tongue motor representations at 1 month (n = 8) or 2 months (n = 7) postextraction, 1 month postimplant placement, and at 1–2 months in naive rats. There were no significant differences across study groups in the onset latencies of the ICMS‐evoked responses (P > 0.05), but in comparison with naive rats, tooth extraction caused a significant (P < 0.05) and sustained (1–2 months) decreased number of ICMS‐defined jaw and tongue sites within face‐M1 and ‐S1, and increased thresholds of ICMS‐evoked responses in these sites. Furthermore, dental implant placement reversed the extraction‐induced changes in face‐S1, and in face‐M1 the number of jaw sites even increased as compared to naive rats. These novel findings suggest that face‐M1 and adjacent face‐S1 may play a role in adaptive mechanisms related to tooth loss and their replacement with dental implants. J. Comp. Neurol. 523:2372–2389, 2015. © 2015 Wiley Periodicals, Inc.  相似文献   
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Mood disorders are often characterised by alterations in circadian rhythms, sleep disturbances and seasonal exacerbation. Conversely, chronobiological treatments utilise zeitgebers for circadian rhythms such as light to improve mood and stabilise sleep, and manipulations of sleep timing and duration as rapid antidepressant modalities. Although sleep deprivation (“wake therapy”) can act within hours, and its mood‐elevating effects be maintained by regular morning light administration/medication/earlier sleep, it has not entered the regular guidelines for treating affective disorders as a first‐line treatment. The hindrances to using chronotherapeutics may lie in their lack of patentability, few sponsors to carry out large multi‐centre trials, non‐reimbursement by medical insurance and their perceived difficulty or exotic “alternative” nature. Future use can be promoted by new technology (single‐sample phase measurements, phone apps, movement and sleep trackers) that provides ambulatory documentation over long periods and feedback to therapist and patient. Light combinations with cognitive behavioural therapy and sleep hygiene practice may speed up and also maintain response. The urgent need for new antidepressants should hopefully lead to reconsideration and implementation of these non‐pharmacological methods, as well as further clinical trials. We review the putative neurochemical mechanisms underlying the antidepressant effect of sleep deprivation and light therapy, and current knowledge linking clocks and sleep with affective disorders: neurotransmitter switching, stress and cortico‐limbic reactivity, clock genes, cortical neuroplasticity, connectomics and neuroinflammation. Despite the complexity of multi‐system mechanisms, more insight will lead to fine tuning and better application of circadian and sleep‐related treatments of depression.  相似文献   
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Single bouts of aerobic exercise can modulate cortical excitability and executive cognitive function, but less is known about the effect of light‐intensity exercise, an intensity of exercise more achievable for certain clinical populations. Fourteen healthy adults (aged 22 to 30) completed the following study procedures twice (≥7 days apart) before and after 30 min of either light aerobic exercise (cycling) or seated rest: neurocognitive battery (multitasking performance, inhibitory control and spatial working memory), paired‐pulse TMS measures of cortical excitability. Significant improvements in response times during multitasking performance and increases in intracortical facilitation (ICF) were seen following light aerobic exercise. Light aerobic exercise can modulate cortical excitability and some executive function tasks. Populations with deficits in multitasking ability may benefit from this intervention.  相似文献   
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Hypothalamic magnocellular neuroendocrine cells have unique electrical properties and a remarkable capacity for morphological and synaptic plasticity. Their large somatic size, their relatively uniform and dense clustering in the supraoptic and paraventricular nuclei, and their large axon terminals in the neurohypophysis make them an attractive target for direct electrophysiological interrogation. Here, we provide a brief review of significant recent findings in the neuroplasticity and neurophysiological properties of these neurones that were presented at the symposium “Electrophysiology of Magnocellular Neurons” during the 13th World Congress on Neurohypophysial Hormones in Ein Gedi, Israel in April 2019. Magnocellular vasopressin (VP) neurones respond directly to hypertonic stimulation with membrane depolarisation, which is triggered by cell shrinkage‐induced opening of an N‐terminal‐truncated variant of transient receptor potential vanilloid type‐1 (TRPV1) channels. New findings indicate that this mechanotransduction depends on actin and microtubule cytoskeletal networks, and that direct coupling of the TRPV1 channels to microtubules is responsible for mechanical gating of the channels. Vasopressin neurones also respond to osmostimulation by activation of epithelial Na+ channels (ENaC). It was shown recently that changes in ENaC activity modulate magnocellular neurone basal firing by generating tonic changes in membrane potential. Both oxytocin and VP neurones also undergo robust excitatory synapse plasticity during chronic osmotic stimulation. Recent findings indicate that new glutamate synapses induced during chronic salt loading express highly labile Ca2+‐permeable GluA1 receptors requiring continuous dendritic protein synthesis for synapse maintenance. Finally, recordings from the uniquely tractable neurohypophysial terminals recently revealed an unexpected property of activity‐dependent neuropeptide release. A significant fraction of the voltage‐dependent neurohypophysial neurosecretion was found to be independent of Ca2+ influx through voltage‐gated Ca2+ channels. Together, these findings provide a snapshot of significant new advances in the electrophysiological signalling mechanisms and neuroplasticity of the hypothalamic‐neurohypophysial system, a system that continues to make important contributions to the field of neurophysiology.  相似文献   
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Objectives. Neurodegenerative diseases like Alzheimer's and Parkinson's Disease, marked by characteristic protein aggregations, are more and more accepted to be synaptic disorders and to arise from a combination of genetic and environmental factors. In this review we propose our concept that neuroplasticity might constitute a link between early life challenges and neurodegeneration. Methods. After introducing the general principles of neuroplasticity, we show how adverse environmental stimuli during development impact adult neuroplasticity and might lead to neurodegenerative processes. Results. There are significant overlaps between neurodevelopmental and neurodegenerative processes. Proteins that represent hallmarks of neurodegeneration are involved in plastic processes under physiological conditions. Brain regions – particularly the hippocampus – that retain life-long plastic capacities are the key targets of neurodegeneration. Neuroplasticity is highest in young age making the brain more susceptible to external influences than later in life. Impacts during critical periods have life-long consequences on neuroplasticity and structural self-organization and are known to be common risk factors for neurodegenerative diseases. Conclusions. Several lines of evidence support a link between developmental neuroplasticity and neurodegenerative processes later in life. A deeper insight into these processes is necessary to design strategies to mitigate or even prevent neurodegenerative pathologies.  相似文献   
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