Neural Plasticity The latest articles from Hindawi © 2017 , Hindawi Limited . All rights reserved. Physical Activity Modulates Common Neuroplasticity Substrates in Major Depressive and Bipolar Disorder Wed, 26 Apr 2017 01:52:01 +0000 Mood disorders (MDs) are chronic, recurrent mental diseases that affect millions of individuals worldwide. Although the biogenic amine model has provided some clinical utility, a need remains to better understand the interrelated mechanisms that contribute to neuroplasticity deficits in MDs and the means by which various therapeutics mitigate them. Of those therapeutics being investigated, physical activity (PA) has shown clear and consistent promise. Accordingly, the aims of this review are to (1) explicate key modulators, processes, and interactions that impinge upon multiple susceptibility points to effectuate neuroplasticity deficits in MDs; (2) explore the putative mechanisms by which PA mitigates these features; (3) review protocols used to induce the positive effects of PA in MDs; and (4) highlight implications for clinicians and researchers. Cristy Phillips Copyright © 2017 Cristy Phillips. All rights reserved. Increased Alpha-Rhythm Dynamic Range Promotes Recovery from Visuospatial Neglect: A Neurofeedback Study Wed, 26 Apr 2017 00:00:00 +0000 Despite recent attempts to use electroencephalogram (EEG) neurofeedback (NFB) as a tool for rehabilitation of motor stroke, its potential for improving neurological impairments of attention—such as visuospatial neglect—remains underexplored. It is also unclear to what extent changes in cortical oscillations contribute to the pathophysiology of neglect, or its recovery. Utilizing EEG-NFB, we sought to causally manipulate alpha oscillations in 5 right-hemisphere stroke patients in order to explore their role in visuospatial neglect. Patients trained to reduce alpha oscillations from their right posterior parietal cortex (rPPC) for 20 minutes daily, over 6 days. Patients demonstrated successful NFB learning between training sessions, denoted by improved regulation of alpha oscillations from rPPC. We observed a significant negative correlation between visuospatial search deficits (i.e., cancellation test) and reestablishment of spontaneous alpha-rhythm dynamic range (i.e., its amplitude variability). Our findings support the use of NFB as a tool for investigating neuroplastic recovery after stroke and suggest reinstatement of intact parietal alpha oscillations as a promising target for reversing attentional deficits. Specifically, we demonstrate for the first time the feasibility of EEG-NFB in neglect patients and provide evidence that targeting alpha amplitude variability might constitute a valuable marker for clinical symptoms and self-regulation. Tomas Ros, Abele Michela, Anne Bellman, Philippe Vuadens, Arnaud Saj, and Patrik Vuilleumier Copyright © 2017 Tomas Ros et al. All rights reserved. Neurorehabilitation: Neural Plasticity and Functional Recovery Thu, 20 Apr 2017 07:24:15 +0000 Toshiyuki Fujiwara, Nam-Jong Paik, and Thomas Platz Copyright © 2017 Toshiyuki Fujiwara et al. All rights reserved. Understanding the Mechanisms of Recovery and/or Compensation following Injury Thu, 20 Apr 2017 00:00:00 +0000 Injury due to stroke and traumatic brain injury result in significant long-term effects upon behavioral functioning. One central question to rehabilitation research is whether the nature of behavioral improvement observed is due to recovery or the development of compensatory mechanisms. The nature of functional improvement can be viewed from the perspective of behavioral changes or changes in neuroanatomical plasticity that follows. Research suggests that these changes correspond to each other in a bidirectional manner. Mechanisms surrounding phenomena like neural plasticity may offer an opportunity to explain how variables such as experience can impact improvement and influence the definition of recovery. What is more, the intensity of the rehabilitative experiences may influence the ability to recover function and support functional improvement of behavior. All of this impacts how researchers, clinicians, and medical professionals utilize rehabilitation. Michael J. Hylin, Abigail L. Kerr, and Ryan Holden Copyright © 2017 Michael J. Hylin et al. All rights reserved. Exercise Modality Is Differentially Associated with Neurocognition in Older Adults Wed, 19 Apr 2017 00:00:00 +0000 This study explored the effects of exercise modality and type of fitness index on cognitive function in the older adults as assessed via behavioral and neuroelectrical approaches. Sixty older adults were assigned to an aerobic exercise, a coordination exercise, or a control group based on their previous exercise experience. The participants completed congruent and incongruent trials of a modified Stroop Test, during which, event-related potentials were recorded. The participants also completed multiple physical tests that assessed health- and skill-related fitness. Our findings suggest that, in general, both aerobic and coordination exercise, as well as higher scores on health- and skill-related fitness indices, are positively associated with better performance of various cognitive functions in the elderly population. The mechanisms underlying these relationships may be differentially related to specific neuroelectrical processes involved in neurocognitive control. Yu-Kai Chang, I-Hua Chu, Jen-Hao Liu, Chih-Han Wu, Chien-Heng Chu, Kao-Teng Yang, and Ai-Guo Chen Copyright © 2017 Yu-Kai Chang et al. All rights reserved. Mechanisms Underlying the Antidepressant Response of Acupuncture via PKA/CREB Signaling Pathway Tue, 18 Apr 2017 00:00:00 +0000 Protein kinase A (PKA)/cAMP response element-binding (CREB) protein signaling pathway, contributing to impaired neurogenesis parallel to depressive-like behaviors, has been identified as the crucial factor involved in the antidepressant response of acupuncture. However, the molecular mechanisms associated with antidepressant response of acupuncture, neurogenesis, and depressive-like behaviors ameliorating remain unexplored. The objective was to identify the mechanisms underlying the antidepressant response of acupuncture through PKA signaling pathway in depression rats by employing the PKA signaling pathway inhibitor H89 in in vivo experiments. Our results indicated that the expression of hippocampal PKA-α and p-CREB was significantly downregulated by chronic unpredicted mild stress (CUMS) procedures. Importantly, acupuncture reversed the downregulation of PKA-α and p-CREB. The expression of PKA-α was upregulated by fluoxetine, but not p-CREB. No significant difference was found between Acu and FLX groups on the expression of PKA-α and p-CREB. Interestingly, H89 inhibited the effects of acupuncture or fluoxetine on upregulating the expression of p-CREB, but not PKA-α. There was no significant difference in expression of CREB among the groups. Conclusively, our findings further support the hypothesis that acupuncture could ameliorate depressive-like behaviors by regulating PKA/CREB signaling pathway, which might be mainly mediated by regulating the phosphorylation level of CREB. Huili Jiang, Xuhui Zhang, Yu Wang, Huimin Zhang, Jing Li, Xinjing Yang, Bingcong Zhao, Chuntao Zhang, Miao Yu, Mingmin Xu, Qiuyun Yu, Xingchen Liang, Xiang Li, Peng Shi, and Tuya Bao Copyright © 2017 Huili Jiang et al. All rights reserved. Therapeutic Potentials of Synapses after Traumatic Brain Injury: A Comprehensive Review Wed, 12 Apr 2017 00:00:00 +0000 Massive studies have focused on the understanding of the pathobiology of cellular and molecular changes and injury mechanisms after traumatic brain injury (TBI), but very few studies have specially discussed the role of synapses in the context of TBI. This paper specifically highlights the role and therapeutic potentials of synapses after TBI. First, we review and conclude how synapses interact with constant structural, metabolic, neuroendocrine, and inflammatory mechanisms after TBI. Second, we briefly describe several key synaptic proteins involved in neuroplasticity, which may be novel neuronal targets for specific intervention. Third, we address therapeutic interventions in association with synapses after TBI. Finally, we concisely discuss the study gaps in the synapses after TBI, in hopes that this would provide more insights for future studies. Synapses play an important role in TBI; while the understandings on the synaptic participation in the treatments and prognosis of TBI are lacking, more studies in this area are warranted. Zunjia Wen, Dong Li, Meifen Shen, and Gang Chen Copyright © 2017 Zunjia Wen et al. All rights reserved. New Treatment Strategies of Depression: Based on Mechanisms Related to Neuroplasticity Tue, 11 Apr 2017 03:00:28 +0000 Major depressive disorder is a severe and complex mental disorder. Impaired neurotransmission and disrupted signalling pathways may influence neuroplasticity, which is involved in the brain dysfunction in depression. Traditional neurobiological theories of depression, such as monoamine hypothesis, cannot fully explain the whole picture of depressive disorders. In this review, we discussed new treatment directions of depression, including modulation of glutamatergic system and noninvasive brain stimulation. Dysfunction of glutamatergic neurotransmission plays an important role in the pathophysiology of depression. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has rapid and lasting antidepressive effects in previous studies. In addition to ketamine, other glutamatergic modulators, such as sarcosine, also show potential antidepressant effect in animal models or clinical trials. Noninvasive brain stimulation is another new treatment strategy beyond pharmacotherapy. Growing evidence has demonstrated that superficial brain stimulations, such as transcranial magnetic stimulation, transcranial direct current stimulation, cranial electrotherapy stimulation, and magnetic seizure therapy, can improve depressive symptoms. The antidepressive effect of these brain stimulations may be through modulating neuroplasticity. In conclusion, drugs that modulate neurotransmission via NMDA receptor and noninvasive brain stimulation may provide new directions of treatment for depression. Furthermore, exploring the underlying mechanisms will help in developing novel therapies for depression in the future. Yu-Jhen Huang, Hsien-Yuan Lane, and Chieh-Hsin Lin Copyright © 2017 Yu-Jhen Huang et al. All rights reserved. Rehabilitation Treatment and Progress of Traumatic Brain Injury Dysfunction Tue, 11 Apr 2017 00:00:00 +0000 Traumatic brain injury (TBI) is a major cause of chronic disability. Worldwide, it is the leading cause of disability in the under 40s. Behavioral problems, mood, cognition, particularly memory, attention, and executive function are commonly impaired by TBI. Spending to assist, TBI survivors with disabilities are estimated to be costly per year. Such impaired functional outcomes following TBI can be improved via various rehabilitative approaches. The objective of the present paper is to review the current rehabilitation treatment of traumatic brain injury in adults. Baoqi Dang, Wenli Chen, Weichun He, and Gang Chen Copyright © 2017 Baoqi Dang et al. All rights reserved. Motor Imagery Impairment in Postacute Stroke Patients Tue, 28 Mar 2017 08:29:30 +0000 Not much is known about how well stroke patients are able to perform motor imagery (MI) and which MI abilities are preserved after stroke. We therefore applied three different MI tasks (one mental chronometry task, one mental rotation task, and one EEG-based neurofeedback task) to a sample of postacute stroke patients () and age-matched healthy controls () for addressing the following questions: First, which of the MI tasks indicate impairment in stroke patients and are impairments restricted to the paretic side? Second, is there a relationship between MI impairment and sensory loss or paresis severity? And third, do the results of the different MI tasks converge? Significant differences between the stroke and control groups were found in all three MI tasks. However, only the mental chronometry task and EEG analysis revealed paresis side-specific effects. Moreover, sensitivity loss contributed to a performance drop in the mental rotation task. The findings indicate that although MI abilities may be impaired after stroke, most patients retain their ability for MI EEG-based neurofeedback. Interestingly, performance in the different MI measures did not strongly correlate, neither in stroke patients nor in healthy controls. We conclude that one MI measure is not sufficient to fully assess an individual’s MI abilities. Niclas Braun, Cornelia Kranczioch, Joachim Liepert, Christian Dettmers, Catharina Zich, Imke Büsching, and Stefan Debener Copyright © 2017 Niclas Braun et al. All rights reserved. Pathological Role of Peptidyl-Prolyl Isomerase Pin1 in the Disruption of Synaptic Plasticity in Alzheimer’s Disease Sun, 26 Mar 2017 00:00:00 +0000 Synaptic loss is the structural basis for memory impairment in Alzheimer’s disease (AD). While the underlying pathological mechanism remains elusive, it is known that misfolded proteins accumulate as β-amyloid (Aβ) plaques and hyperphosphorylated Tau tangles decades before the onset of clinical disease. The loss of Pin1 facilitates the formation of these misfolded proteins in AD. Pin1 protein controls cell-cycle progression and determines the fate of proteins by the ubiquitin proteasome system. The activity of the ubiquitin proteasome system directly affects the functional and structural plasticity of the synapse. We localized Pin1 to dendritic rafts and postsynaptic density (PSD) and found the pathological loss of Pin1 within the synapses of AD brain cortical tissues. The loss of Pin1 activity may alter the ubiquitin-regulated modification of PSD proteins and decrease levels of Shank protein, resulting in aberrant synaptic structure. The loss of Pin1 activity, induced by oxidative stress, may also render neurons more susceptible to the toxicity of oligomers of Aβ and to excitation, thereby inhibiting NMDA receptor-mediated synaptic plasticity and exacerbating NMDA receptor-mediated synaptic degeneration. These results suggest that loss of Pin1 activity could lead to the loss of synaptic plasticity in the development of AD. Lingyan Xu, Zhiyun Ren, Frances E. Chow, Richard Tsai, Tongzheng Liu, Flavio Rizzolio, Silvia Boffo, Yungen Xu, Shaohui Huang, Carol F. Lippa, and Yuesong Gong Copyright © 2017 Lingyan Xu et al. All rights reserved. Electrophysiological, Morphological, and Ultrastructural Features of the Injured Spinal Cord Tissue after Transplantation of Human Umbilical Cord Blood Mononuclear Cells Genetically Modified with the VEGF and GDNF Genes Tue, 21 Mar 2017 00:00:00 +0000 In this study, we examined the efficacy of human umbilical cord blood mononuclear cells (hUCB-MCs), genetically modified with the VEGF and GDNF genes using adenoviral vectors, on posttraumatic regeneration after transplantation into the site of spinal cord injury (SCI) in rats. Thirty days after SCI, followed by transplantation of nontransduced hUCB-MCs, we observed an improvement in (latency period, LP) and waves, compared to the group without therapy after SCI. For genetically modified hUCB-MCs, there was improvement in of wave and LP of both the and waves. The ratio between of the and waves () demonstrated that transplantation into the area of SCI of genetically modified hUCB-MCs was more effective than nontransduced hUCB-MCs. Spared tissue and myelinated fibers were increased at day 30 after SCI and transplantation of hUCB-MCs in the lateral and ventral funiculi 2.5 mm from the lesion epicenter. Transplantation of hUCB-MCs genetically modified with the VEGF and GNDF genes significantly increased the number of spared myelinated fibers (22-fold, ) in the main corticospinal tract compared to the nontransduced ones. HNA+ cells with the morphology of phagocytes and microglia-like cells were found as compact clusters or cell bridges within the traumatic cavities that were lined by GFAP+ host astrocytes. Our results show that hUCB-MCs transplanted into the site of SCI improved regeneration and that hUCB-MCs genetically modified with the VEGF and GNDF genes were more effective than nontransduced hUCB-MCs. Y. O. Mukhamedshina, Z. E. Gilazieva, S. S. Arkhipova, L. R. Galieva, E. E. Garanina, A. A. Shulman, G. G. Yafarova, Y. A. Chelyshev, N. V. Shamsutdinova, and A. A. Rizvanov Copyright © 2017 Y. O. Mukhamedshina et al. All rights reserved. Distinct Pattern of Microgliosis in the Olfactory Bulb of Neurodegenerative Proteinopathies Sun, 19 Mar 2017 09:07:19 +0000 The olfactory bulb (OB) shows early neuropathological hallmarks in numerous neurodegenerative diseases, for example, in Alzheimer’s disease (AD) and Parkinson’s disease (PD). The glomerular and granular cell layer of the OB is characterized by preserved cellular plasticity in the adult brain. In turn, alterations of this cellular plasticity are related to neuroinflammation such as microglia activation, implicated in the pathogenesis of AD and PD, as well as frontotemporal lobe degeneration (FTLD). To determine microglia proliferation and activation we analyzed ionized calcium binding adaptor molecule 1 (Iba1) expressing microglia in the glomerular and granular cell layer, and the olfactory tract of the OB from patients with AD, PD dementia/dementia with Lewy bodies (PDD/DLB), and FTLD compared to age-matched controls. The number of Iba1 and CD68 positive microglia associated with enlarged amoeboid microglia was increased particularly in AD, to a lesser extent in FTLD and PDD/DLB as well, while the proportion of proliferating microglia was not altered. In addition, cells expressing the immature neuronal marker polysialylated neural cell adhesion molecule (PSA-NCAM) were increased in the glomerular layer of PDD/DLB and FTLD cases only. These findings provide novel and detailed insights into differential levels of microglia activation in the OB of neurodegenerative diseases. Zacharias Kohl, Johannes C. M. Schlachetzki, Judith Feldewerth, Philipp Hornauer, Martina Münch, Anthony Adame, Markus J. Riemenschneider, Jürgen Winkler, and Eliezer Masliah Copyright © 2017 Zacharias Kohl et al. All rights reserved. Thalamocortical Connectivity and Microstructural Changes in Congenital and Late Blindness Mon, 13 Mar 2017 08:19:45 +0000 There is ample evidence that the occipital cortex of congenitally blind individuals processes nonvisual information. It remains a debate whether the cross-modal activation of the occipital cortex is mediated through the modulation of preexisting corticocortical projections or the reorganisation of thalamocortical connectivity. Current knowledge on this topic largely stems from anatomical studies in animal models. The aim of this study was to test whether purported changes in thalamocortical connectivity in blindness can be revealed by tractography based on diffusion-weighted magnetic resonance imaging. To assess the thalamocortical network, we used a clustering method based on the thalamic white matter projections towards predefined cortical regions. Five thalamic clusters were obtained in each group representing their cortical projections. Although we did not find differences in the thalamocortical network between congenitally blind individuals, late blind individuals, and normal sighted controls, diffusion tensor imaging (DTI) indices revealed significant microstructural changes within thalamic clusters of both blind groups. Furthermore, we find a significant decrease in fractional anisotropy (FA) in occipital and temporal thalamocortical projections in both blind groups that were not captured at the network level. This suggests that plastic microstructural changes have taken place, but not in a degree to be reflected in the tractography-based thalamocortical network. N. H. Reislev, T. B. Dyrby, H. R. Siebner, H. Lundell, M. Ptito, and R. Kupers Copyright © 2017 N. H. Reislev et al. All rights reserved. Assessed and Emerging Biomarkers in Stroke and Training-Mediated Stroke Recovery: State of the Art Wed, 08 Mar 2017 00:00:00 +0000 Since the increasing update of the biomolecular scientific literature, biomarkers in stroke have reached an outstanding and remarkable revision in the very recent years. Besides the diagnostic and prognostic role of some inflammatory markers, many further molecules and biological factors have been added to the list, including tissue derived cytokines, growth factor-like molecules, hormones, and microRNAs. The literatures on brain derived growth factor and other neuroimmune mediators, bone-skeletal muscle biomarkers, cellular and immunity biomarkers, and the role of microRNAs in stroke recovery were reviewed. To date, biomarkers represent a possible challenge in the diagnostic and prognostic evaluation of stroke onset, pathogenesis, and recovery. Many molecules are still under investigation and may become promising and encouraging biomarkers. Experimental and clinical research should increase this list and promote new discoveries in this field, to improve stroke diagnosis and treatment. Marialuisa Gandolfi, Nicola Smania, Antonio Vella, Alessandro Picelli, and Salvatore Chirumbolo Copyright © 2017 Marialuisa Gandolfi et al. All rights reserved. Evidence of Presynaptic Localization and Function of the c-Jun N-Terminal Kinase Tue, 07 Mar 2017 00:00:00 +0000 The c-Jun N-terminal kinase (JNK) is part of a stress signalling pathway strongly activated by NMDA-stimulation and involved in synaptic plasticity. Many studies have been focused on the post-synaptic mechanism of JNK action, and less is known about JNK presynaptic localization and its physiological role at this site. Here we examined whether JNK is present at the presynaptic site and its activity after presynaptic NMDA receptors stimulation. By using N-SIM Structured Super Resolution Microscopy as well as biochemical approaches, we demonstrated that presynaptic fractions contained significant amount of JNK protein and its activated form. By means of modelling design, we found that JNK, via the JBD domain, acts as a physiological effector on T-SNARE proteins; then using biochemical approaches we demonstrated the interaction between Syntaxin-1-JNK, Syntaxin-2-JNK, and Snap25-JNK. In addition, taking advance of the specific JNK inhibitor peptide, D-JNKI1, we defined JNK action on the SNARE complex formation. Finally, electrophysiological recordings confirmed the role of JNK in the presynaptic modulation of vesicle release. These data suggest that JNK-dependent phosphorylation of T-SNARE proteins may have an important functional role in synaptic plasticity. Silvia Biggi, Lucia Buccarello, Alessandra Sclip, Pellegrino Lippiello, Noemi Tonna, Cristiano Rumio, Daniele Di Marino, Maria Concetta Miniaci, and Tiziana Borsello Copyright © 2017 Silvia Biggi et al. All rights reserved. Circadian Plasticity of Mammalian Inhibitory Interneurons Mon, 06 Mar 2017 09:46:19 +0000 Inhibitory interneurons participate in all neuronal circuits in the mammalian brain, including the circadian clock system, and are indispensable for their effective function. Although the clock neurons have different molecular and electrical properties, their main function is the generation of circadian oscillations. Here we review the circadian plasticity of GABAergic interneurons in several areas of the mammalian brain, suprachiasmatic nucleus, neocortex, hippocampus, olfactory bulb, cerebellum, striatum, and in the retina. Malgorzata Jasinska and Elzbieta Pyza Copyright © 2017 Malgorzata Jasinska and Elzbieta Pyza. All rights reserved. Changes in Cortical Activation Patterns in Language Areas following an Aerobic Exercise Intervention in Older Adults Mon, 06 Mar 2017 00:00:00 +0000 Previous work has shown that older adults who evidence increased right inferior frontal gyrus (IFG) activity during language tasks show decreased sematic verbal fluency performance. The current study sought to evaluate if an aerobic exercise intervention can alter patterns of brain activity during a semantic verbal fluency task assessed by functional magnetic resonance imaging (fMRI). Thirty-two community-dwelling, sedentary older adults were enrolled to a 12-week aerobic “Spin” exercise group or a 12-week nonaerobic exercise control condition (Balance). Thirty participants completed their assigned intervention (16 Spin; 14 Balance) with pre- and postintervention assessments of a semantic verbal fluency task during fMRI and estimated VO2max testing. There was a significant increase in the change scores for estimated VO2max of the Spin group when compared to the Balance group. Semantic verbal fluency output within the scanner was also improved in the Spin group as compared to controls at postassessment. Group fMRI comparisons of IFG activity showed lower activity in the right IFG following the intervention in the aerobic Spin group when compared to the Balance group. Regression analysis of imaging data with change in both estimated VO2max and semantic verbal fluency was negatively correlated with activity in right IFG. The current work is registered as clinical trial with NCT01787292 and NCT02787655. Joe Nocera, Bruce Crosson, Kevin Mammino, and Keith M. McGregor Copyright © 2017 Joe Nocera et al. All rights reserved. Aerobic Exercise Effects on Ocular Dominance Plasticity with a Phase Combination Task in Human Adults Sun, 05 Mar 2017 08:14:14 +0000 Several studies have shown that short-term monocular patching can induce ocular dominance plasticity in normal adults, in which the patched eye becomes stronger in binocular viewing. There is a recent study showing that exercise enhances this plasticity effect when assessed with binocular rivalry. We address one question, is this enhancement from exercise a general effect such that it is seen for measures of binocular processing other than that revealed using binocular rivalry? Using a binocular phase combination task in which we directly measure each eye’s contribution to the binocularly fused percept, we show no additional effect of exercise after short-term monocular occlusion and argue that the enhancement of ocular dominance plasticity from exercise could not be demonstrated with our approach. Jiawei Zhou, Alexandre Reynaud, and Robert F. Hess Copyright © 2017 Jiawei Zhou et al. All rights reserved. Intrahemispheric Perfusion in Chronic Stroke-Induced Aphasia Sun, 05 Mar 2017 00:00:00 +0000 Stroke-induced alterations in cerebral blood flow (perfusion) may contribute to functional language impairments and recovery in chronic aphasia. Using MRI, we examined perfusion in the right and left hemispheres of 35 aphasic and 16 healthy control participants. Across 76 regions (38 per hemisphere), no significant between-subjects differences were found in the left, whereas blood flow in the right was increased in the aphasic compared to the control participants. Region-of-interest (ROI) analyses showed a varied pattern of hypo- and hyperperfused regions across hemispheres in the aphasic participants; however, there were no significant correlations between perfusion values and language abilities in these regions. These patterns may reflect autoregulatory changes in blood flow following stroke and/or increases in general cognitive effort, rather than maladaptive language processing. We also examined blood flow in perilesional tissue, finding the greatest hypoperfusion close to the lesion (within 0–6 mm), with greater hypoperfusion in this region compared to more distal regions. In addition, hypoperfusion in this region was significantly correlated with language impairment. These findings underscore the need to consider cerebral perfusion as a factor contributing to language deficits in chronic aphasia as well as recovery of language function. Cynthia K. Thompson, Matthew Walenski, YuFen Chen, David Caplan, Swathi Kiran, Brenda Rapp, Kristin Grunewald, Mia Nunez, Richard Zinbarg, and Todd B. Parrish Copyright © 2017 Cynthia K. Thompson et al. All rights reserved. Understanding Neuromuscular System Plasticity to Improve Motor Function in Health, Disease, and Injury Thu, 02 Mar 2017 08:57:55 +0000 Guang H. Yue, Brian C. Clark, Sheng Li, and David E. Vaillancourt Copyright © 2017 Guang H. Yue et al. All rights reserved. Corrigendum to “Dopaminergic Modulation of Striatal Inhibitory Transmission and Long-Term Plasticity” Thu, 02 Mar 2017 06:37:41 +0000 Elizabeth Nieto-Mendoza and Elizabeth Hernández-Echeagaray Copyright © 2017 Elizabeth Nieto-Mendoza and Elizabeth Hernández-Echeagaray. All rights reserved. Effects of Traumatic Stress Induced in the Juvenile Period on the Expression of Gamma-Aminobutyric Acid Receptor Type A Subunits in Adult Rat Brain Thu, 02 Mar 2017 00:00:00 +0000 Studies have found that early traumatic experience significantly increases the risk of posttraumatic stress disorder (PTSD). Gamma-aminobutyric acid (GABA) deficits were proposed to be implicated in development of PTSD, but the alterations of GABA receptor A (GABAAR) subunits induced by early traumatic stress have not been fully elucidated. Furthermore, previous studies suggested that exercise could be more effective than medications in reducing severity of anxiety and depression but the mechanism is unclear. This study used inescapable foot-shock to induce PTSD in juvenile rats and examined their emotional changes using open-field test and elevated plus maze, memory changes using Morris water maze, and the expression of GABAAR subunits (γ2, α2, and α5) in subregions of the brain in the adulthood using western blotting and immunohistochemistry. We aimed to observe the role of GABAAR subunits changes induced by juvenile trauma in the pathogenesis of subsequent PTSD in adulthood. In addition, we investigated the protective effects of exercise for 6 weeks and benzodiazepine (clonazepam) for 2 weeks. This study found that juvenile traumatic stress induced chronic anxiety and spatial memory loss and reduced expression of GABAAR subunits in the adult rat brains. Furthermore, exercise led to significant improvement as compared to short-term BZ treatment. Cui Yan Lu, De Xiang Liu, Hong Jiang, Fang Pan, Cyrus S. H. Ho, and Roger C. M. Ho Copyright © 2017 Cui Yan Lu et al. All rights reserved. Imaging Neural Plasticity following Brain Injury Tue, 28 Feb 2017 15:57:04 +0000 Lijun Bai, Lin Ai, and Kevin K. W. Wang Copyright © 2017 Lijun Bai et al. All rights reserved. Effect of Illumination on Ocular Status Modifications Induced by Short-Term 3D TV Viewing Mon, 27 Feb 2017 11:43:39 +0000 Objectives. This study aimed to compare changes in ocular status after 3D TV viewing under three modes of illumination and thereby identify optimal illumination for 3D TV viewing. Methods. The following measures of ocular status were assessed: the accommodative response, accommodative microfluctuation, accommodative facility, relative accommodation, gradient accommodative convergence/accommodation (AC/A) ratio, phoria, and fusional vergence. The observers watched 3D television for 90 minutes through 3D shutter glasses under three illumination modes: A, complete darkness; B, back illumination (50 lx); and C, front illumination (130 lx). The ocular status of the observers was assessed both before and after the viewing. Results. After 3D TV viewing, the accommodative response and accommodative microfluctuation were significantly changed under illumination Modes A and B. The near positive fusional vergence decreased significantly after the 90-minute 3D viewing session under each illumination mode, and this effect was not significantly different among the three modes. Conclusions. Short-term 3D viewing modified the ocular status of adults. The least amount of such change occurred with front illumination, suggesting that this type of illumination is an appropriate mode for 3D shutter TV viewing. Yuanyuan Chen, Yuwen Wang, Xinping Yu, Aiqin Xu, Jian Jiang, and Hao Chen Copyright © 2017 Yuanyuan Chen et al. All rights reserved. Emerging Synaptic Molecules as Candidates in the Etiology of Neurological Disorders Sun, 26 Feb 2017 08:14:19 +0000 Synapses are complex structures that allow communication between neurons in the central nervous system. Studies conducted in vertebrate and invertebrate models have contributed to the knowledge of the function of synaptic proteins. The functional synapse requires numerous protein complexes with specialized functions that are regulated in space and time to allow synaptic plasticity. However, their interplay during neuronal development, learning, and memory is poorly understood. Accumulating evidence links synapse proteins to neurodevelopmental, neuropsychiatric, and neurodegenerative diseases. In this review, we describe the way in which several proteins that participate in cell adhesion, scaffolding, exocytosis, and neurotransmitter reception from presynaptic and postsynaptic compartments, mainly from excitatory synapses, have been associated with several synaptopathies, and we relate their functions to the disease phenotype. Viviana I. Torres, Daniela Vallejo, and Nibaldo C. Inestrosa Copyright © 2017 Viviana I. Torres et al. All rights reserved. Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model Thu, 23 Feb 2017 11:20:27 +0000 Birth asphyxia also termed perinatal asphyxia is an obstetric complication that strongly affects brain structure and function. Central nervous system is highly susceptible to oxidative damage caused by perinatal asphyxia while activation and maturity of the proper pathways are relevant to avoiding abnormal neural development. Perinatal asphyxia is associated with high morbimortality in term and preterm neonates. Although several studies have demonstrated a variety of biochemical and molecular pathways involved in perinatal asphyxia physiopathology, little is known about the synaptic alterations induced by perinatal asphyxia. Nearly 25% of the newborns who survive perinatal asphyxia develop neurological disorders such as cerebral palsy and certain neurodevelopmental and learning disabilities where synaptic connectivity disturbances may be involved. Accordingly, here we review and discuss the association of possible synaptic dysfunction with perinatal asphyxia on the basis of updated evidence from an experimental model. María Inés Herrera, Matilde Otero-Losada, Lucas Daniel Udovin, Carlos Kusnier, Rodolfo Kölliker-Frers, Wanderley de Souza, and Francisco Capani Copyright © 2017 María Inés Herrera et al. All rights reserved. Predictors of Recovery from Traumatic Brain Injury-Induced Prolonged Consciousness Disorder Thu, 23 Feb 2017 11:13:20 +0000 We investigated the clinical predictors of the degree of recovery in patients with prolonged disorders of consciousness (PDC) caused by traumatic brain injury. Fourteen patients with PDC underwent two diffusion tensor imaging (DTI) studies; the first and second scans were performed at and days after the injury, respectively. In addition to the temporal changes in each of these diffusion parameters, fractional anisotropy (FA), mean diffusivity, axial diffusivity (AD), and radial diffusivity were assessed over a 1-year period. Relationship of clinical and DTI parameters with recovery from PDC (RPDC) was evaluated using Spearman’s rank-correlation and stepwise multiple linear regression analysis. The mean FA and number of voxels with FA values > 0.4 (VsFA0.4) were significantly decreased at the second scan. A significant positive correlation was observed between the degree of RPDC and mean FA () and VsFA0.4 () as well as between the difference in VsFA0.4 () and AD () between the first and second scans. On multiple linear regression analysis, initial severity of PDC and the difference in AD remained significantly associated with the degree of RPDC. The microstructural white matter changes observed in this study indicate their potential relation with the degree of RPDC over the longer term. Hiroaki Abe, Keigo Shimoji, Yoshihide Nagamine, Satoru Fujiwara, and Shin-Ichi Izumi Copyright © 2017 Hiroaki Abe et al. All rights reserved. Fatigue and Muscle Strength Involving Walking Speed in Parkinson’s Disease: Insights for Developing Rehabilitation Strategy for PD Wed, 22 Feb 2017 13:20:20 +0000 Background. Problems with gait in Parkinson’s disease (PD) are a challenge in neurorehabilitation, partly because the mechanisms causing the walking disability are unclear. Weakness and fatigue, which may significantly influence gait, are commonly reported by patients with PD. Hence, the aim of this study was to investigate the association between weakness and fatigue and walking ability in patients with PD. Methods. We recruited 25 patients with idiopathic PD and 25 age-matched healthy adults. The maximum voluntary contraction (MVC), twitch force, and voluntary activation levels were measured before and after a knee fatigue exercise. General fatigue, central fatigue, and peripheral fatigue were quantified by exercise-induced changes in MVC, twitch force, and activation level. In addition, subjective fatigue was measured using the Multidimensional Fatigue Inventory (MFI) and Fatigue Severity Scale (FSS). Results. The patients with PD had lower activation levels, more central fatigue, and more subjective fatigue than the healthy controls. There were no significant differences in twitch force or peripheral fatigue index between the two groups. The reduction in walking speed was related to the loss of peripheral strength and PD itself. Conclusion. Fatigue and weakness of central origin were related to PD, while peripheral strength was important for walking ability. The results suggest that rehabilitation programs for PD should focus on improving both central and peripheral components of force. Ying-Zu Huang, Fang-Yu Chang, Wei-Chia Liu, Yu-Fen Chuang, Li-Ling Chuang, and Ya-Ju Chang Copyright © 2017 Ying-Zu Huang et al. All rights reserved. The Impact of Feedback on the Different Time Courses of Multisensory Temporal Recalibration Tue, 21 Feb 2017 07:06:30 +0000 The capacity to rapidly adjust perceptual representations confers a fundamental advantage when confronted with a constantly changing world. Unexplored is how feedback regarding sensory judgments (top-down factors) interacts with sensory statistics (bottom-up factors) to drive long- and short-term recalibration of multisensory perceptual representations. Here, we examined the time course of both cumulative and rapid temporal perceptual recalibration for individuals completing an audiovisual simultaneity judgment task in which they were provided with varying degrees of feedback. We find that in the presence of feedback (as opposed to simple sensory exposure) temporal recalibration is more robust. Additionally, differential time courses are seen for cumulative and rapid recalibration dependent upon the nature of the feedback provided. Whereas cumulative recalibration effects relied more heavily on feedback that informs (i.e., negative feedback) rather than confirms (i.e., positive feedback) the judgment, rapid recalibration shows the opposite tendency. Furthermore, differential effects on rapid and cumulative recalibration were seen when the reliability of feedback was altered. Collectively, our findings illustrate that feedback signals promote and sustain audiovisual recalibration over the course of cumulative learning and enhance rapid trial-to-trial learning. Furthermore, given the differential effects seen for cumulative and rapid recalibration, these processes may function via distinct mechanisms. Matthew A. De Niear, Jean-Paul Noel, and Mark T. Wallace Copyright © 2017 Matthew A. De Niear et al. All rights reserved.