Aerobic exercise improves cognitive and motor function by inducing neural changes detected using molecular, cellular, and systems level neuroscience techniques. This review unifies the knowledge ...gained across various neuroscience techniques to provide a comprehensive profile of the neural mechanisms that mediate exercise-induced neuroplasticity. Using a model of exercise-induced neuroplasticity, this review emphasizes the sequence of neural events that accompany exercise, and ultimately promote changes in human performance. This is achieved by differentiating between neuroplasticity induced by acute versus chronic aerobic exercise. Furthermore, this review emphasizes experimental considerations that influence the opportunity to observe exercise-induced neuroplasticity in humans. These include modifiable factors associated with the exercise intervention and nonmodifiable factors such as biological sex, ovarian hormones, genetic variations, and fitness level. To maximize the beneficial effects of exercise in health, disease, and following injury, future research should continue to explore the mechanisms that mediate exercise-induced neuroplasticity. This review identifies some fundamental gaps in knowledge that may serve to guide future research in this area.
Astrocyte roles in traumatic brain injury Burda, Joshua E.; Bernstein, Alexander M.; Sofroniew, Michael V.
Experimental neurology,
01/2016, Letnik:
275, Številka:
3
Journal Article
Recenzirano
Odprti dostop
Astrocytes sense changes in neural activity and extracellular space composition. In response, they exert homeostatic mechanisms critical for maintaining neural circuit function, such as buffering ...neurotransmitters, modulating extracellular osmolarity and calibrating neurovascular coupling. In addition to upholding normal brain activities, astrocytes respond to diverse forms of brain injury with heterogeneous and progressive changes of gene expression, morphology, proliferative capacity and function that are collectively referred to as reactive astrogliosis. Traumatic brain injury (TBI) sets in motion complex events in which noxious mechanical forces cause tissue damage and disrupt central nervous system (CNS) homeostasis, which in turn trigger diverse multi-cellular responses that evolve over time and can lead either to neural repair or secondary cellular injury. In response to TBI, astrocytes in different cellular microenvironments tune their reactivity to varying degrees of axonal injury, vascular disruption, ischemia and inflammation. Here we review different forms of TBI-induced astrocyte reactivity and the functional consequences of these responses for TBI pathobiology. Evidence regarding astrocyte contribution to post-traumatic tissue repair and synaptic remodeling is examined, and the potential for targeting specific aspects of astrogliosis to ameliorate TBI sequelae is considered.
•Astrocytes respond to diverse forms of TBI with changes of gene expression, morphology, proliferation and function.•Astrocytes tune their reactivity to varying degrees of axonal and vascular injury, ischemia and inflammation after TBI.•Astrocytes regulate brain inflammation and blood-brain barrier permeability after TBI.•Astrocytes significantly contribute to post-traumatic tissue repair and synaptic remodeling following TBI.
Brain‐inspired electronics with multimodal signal processing have been investigated as the next‐generation semiconductor platforms owing to the limitations of von Neumann architecture, which limits ...data processing and energy consumption efficiencies. This study demonstrates the molecular reconfiguration of plasticity of artificial synaptic devices with tunable electric conductance based on molecular dynamics at the channel surfaces for realizing chemical multimodality. Carrier transport dynamics are adjusted using the density of trapped carriers for the molecular adsorption of HS in the MoSe2 channel, and the results are consistent with the molecular simulations. In molecular dynamics‐controlled devices, enhanced hysteresis enables the engineering of artificial neuroplasticity, mimicking the neurotransmitter release of biological synapses. Owing to the molecular reconfigurability of MoSe2 devices, the synaptic weights of excitatory and inhibitory synapse modes are significantly enhanced. Thus, this study can potentially contribute to the creation of the next generation of multimodal interfaces and artificial intelligence hardware realization.
Molecular adsorption at the surface of channels induces the pulling or repelling of carriers transferred across the 2D semiconductor channel, which enables bioinspired synaptic behavior owing to the trapping or de‐trapping of carriers. Molecularly reconfigurable surface engineering in MoSe2 FETs is employed to mimic and enhance the essential features of biological synapses using van der Waals interactions upon molecular adsorption.
Proper integration of different inputs targeting the dendritic tree of CA3 pyramidal cells (CA3PCs) is critical for associative learning and recall. Dendritic Ca.sup.2+ spikes have been proposed to ...perform associative computations in other PC types by detecting conjunctive activation of different afferent input pathways, initiating afterdepolarization (ADP), and triggering burst firing. Implementation of such operations fundamentally depends on the actual biophysical properties of dendritic Ca.sup.2+ spikes; yet little is known about these properties in dendrites of CA3PCs. Using dendritic patch-clamp recordings and two-photon Ca.sup.2+ imaging in acute slices from male rats, we report that, unlike CA1PCs, distal apical trunk dendrites of CA3PCs exhibit distinct forms of dendritic Ca.sup.2+ spikes. Besides ADP-type global Ca.sup.2+ spikes, a majority of dendrites expresses a novel, fast Ca.sup.2+ spike type that is initiated locally without bAPs, can recruit additional Na.sup.+ currents, and is compartmentalized to the activated dendritic subtree. Occurrence of the different Ca.sup.2+ spike types correlates with dendritic structure, indicating morpho-functional heterogeneity among CA3PCs. Importantly, ADPs and dendritically initiated spikes produce opposing somatic output: bursts versus strictly single-action potentials, respectively. The uncovered variability of dendritic Ca.sup.2+ spikes may underlie heterogeneous input-output transformation and bursting properties of CA3PCs, and might specifically contribute to key associative and non-associative computations performed by the CA3 network.
During the aging process, physical capabilities (e.g., muscular strength) and cognitive functions (e.g., memory) gradually decrease. Regarding cognitive functions, substantial functional (e.g., ...compensatory brain activity) and structural changes (e.g., shrinking of the hippocampus) in the brain cause this decline. Notably, growing evidence points towards a relationship between cognition and measures of muscular strength and muscle mass. Based on this emerging evidence, resistance exercises and/or resistance training, which contributes to the preservation and augmentation of muscular strength and muscle mass, may trigger beneficial neurobiological processes and could be crucial for healthy aging that includes preservation of the brain and cognition. Compared with the multitude of studies that have investigated the influence of endurance exercises and/or endurance training on cognitive performance and brain structure, considerably less work has focused on the effects of resistance exercises and/or resistance training. While the available evidence regarding resistance exercise-induced changes in cognitive functions is pooled, the underlying neurobiological processes, such as functional and structural brain changes, have yet to be summarized. Hence, the purpose of this systematic review is to provide an overview of resistance exercise-induced functional and/or structural brain changes that are related to cognitive functions.
A systematic literature search was conducted by two independent researchers across six electronic databases; 5957 records were returned, of which 18 were considered relevant and were analyzed.
Based on our analyses, resistance exercises and resistance training evoked substantial functional brain changes, especially in the frontal lobe, which were accompanied by improvements in executive functions. Furthermore, resistance training led to lower white matter atrophy and smaller white matter lesion volumes. However, based on the relatively small number of studies available, the findings should be interpreted cautiously. Hence, future studies are required to investigate the underlying neurobiological mechanisms and to verify whether the positive findings can be confirmed and transferred to other needy cohorts, such as older adults with dementia, sarcopenia and/or dynapenia.
ABSTRACT
Interventions that preserve motor neurons or restore functional motor neuroplasticity may extend longevity in amyotrophic lateral sclerosis (ALS). Delivery of neurotrophins may potentially ...revive degenerating motor neurons, yet this approach is dependent on the proper subcellular localization of neurotrophin receptor (NTR) to plasmalemmal signaling microdomains, termed membrane/lipid rafts (MLRs). We previously showed that over‐expression of synapsin‐driven caveolin‐1 (Cav‐1) (SynCav1) increases MLR localization of NTR e.g., receptor tyrosine kinase B (TrkB), promotes hippocampal synaptic and neuroplasticity, and significantly improves learning and memory in aged mice. The present study crossed a SynCav1 transgene‐positive (SynCav1+) mouse with the mutant human superoxide dismutase glycine to alanine point mutation at amino acid 93 (hSOD1G93A) mouse model of ALS. When compared with hSOD1G93A, hSOD1G93A/SynCav1+ mice exhibited greater body weight and longer survival as well as better motor function. Microscopic analyses of hSOD1G93A/SynCav1+ spinal cords revealed preserved spinal cord α‐motor neurons and preserved mitochondrial morphology. Moreover, hSOD1G93A/SynCav1+ spinal cords contained more MLRs (cholera toxin subunit B positive) and MLR‐associated TrkB and Cav‐1 protein expression. These findings demonstrate that SynCav1 delays disease progression in a mouse model of ALS, potentially by preserving or restoring NTR expression and localization to MLRs.—Sawada, A., Wang, S., Jian, M., Leem, J., Wackerbarth, J., Egawa, J., Schilling, J. M., Platoshyn, O., Zemljic‐Harpf, A., Roth, D. M., Patel, H. H., Patel, P. M., Marsala, M., Head, B. P. Neuron‐targeted caveolin‐1 improves neuromuscular function and extends survival in SOD1G93A mice. FASEB J. 33, 7545–7554 (2019). www.fasebj.org
This review explores cross-modal cortical plasticity as a result of auditory deprivation in populations with hearing loss across the age spectrum, from development to adulthood. Cross-modal ...plasticity refers to the phenomenon when deprivation in one sensory modality (e.g. the auditory modality as in deafness or hearing loss) results in the recruitment of cortical resources of the deprived modality by intact sensory modalities (e.g. visual or somatosensory systems). We discuss recruitment of auditory cortical resources for visual and somatosensory processing in deafness and in lesser degrees of hearing loss. We describe developmental cross-modal re-organization in the context of congenital or pre-lingual deafness in childhood and in the context of adult-onset, age-related hearing loss, with a focus on how cross-modal plasticity relates to clinical outcomes. We provide both single-subject and group-level evidence of cross-modal re-organization by the visual and somatosensory systems in bilateral, congenital deafness, single-sided deafness, adults with early-stage, mild-moderate hearing loss, and individual adult and pediatric patients exhibit excellent and average speech perception with hearing aids and cochlear implants. We discuss a framework in which changes in cortical resource allocation secondary to hearing loss results in decreased intra-modal plasticity in auditory cortex, accompanied by increased cross-modal recruitment of auditory cortices by the other sensory systems, and simultaneous compensatory activation of frontal cortices. The frontal cortices, as we will discuss, play an important role in mediating cognitive compensation in hearing loss. Given the wide range of variability in behavioral performance following audiological intervention, changes in cortical plasticity may play a valuable role in the prediction of clinical outcomes following intervention. Further, the development of new technologies and rehabilitation strategies that incorporate brain-based biomarkers may help better serve hearing impaired populations across the lifespan.
•We describe evidence of cross-modal plasticity by vision and somatosenation in children and adults with hearing loss.•We describe evidence of compensatory activation of frontal cortices in hearing loss.•We describe applications of cross-modal plasticity in clinical populations with hearing loss.
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