Neural Plasticity The latest articles from Hindawi © 2017 , Hindawi Limited . All rights reserved. Could LC-NE-Dependent Adjustment of Neural Gain Drive Functional Brain Network Reorganization? Sun, 21 May 2017 00:00:00 +0000 The locus coeruleus-norepinephrine (LC-NE) system is thought to act at synaptic, cellular, microcircuit, and network levels to facilitate cognitive functions through at least two different processes, not mutually exclusive. Accordingly, as a reset signal, the LC-NE system could trigger brain network reorganizations in response to salient information in the environment and/or adjust the neural gain within its target regions to optimize behavioral responses. Here, we provide evidence of the co-occurrence of these two mechanisms at the whole-brain level, in resting-state conditions following a pharmacological stimulation of the LC-NE system. We propose that these two mechanisms are interdependent such that the LC-NE-dependent adjustment of the neural gain inferred from the clustering coefficient could drive functional brain network reorganizations through coherence in the gamma rhythm. Via the temporal dynamic of gamma-range band-limited power, the release of NE could adjust the neural gain, promoting interactions only within the neuronal populations whose amplitude envelopes are correlated, thus making it possible to reorganize neuronal ensembles, functional networks, and ultimately, behavioral responses. Thus, our proposal offers a unified framework integrating the putative influence of the LC-NE system on both local- and long-range adjustments of brain dynamics underlying behavioral flexibility. Carole Guedj, David Meunier, Martine Meunier, and Fadila Hadj-Bouziane Copyright © 2017 Carole Guedj et al. All rights reserved. Noradrenergic Modulation of Cognition in Health and Disease Wed, 17 May 2017 08:06:12 +0000 Norepinephrine released by the locus coeruleus modulates cellular processes and synaptic transmission in the central nervous system through its actions at a number of pre- and postsynaptic receptors. This transmitter system facilitates sensory signal detection and promotes waking and arousal, processes which are necessary for navigating a complex and dynamic sensory environment. In addition to its effects on sensory processing and waking behavior, norepinephrine is now recognized as a contributor to various aspects of cognition, including attention, behavioral flexibility, working memory, and long-term mnemonic processes. Two areas of dense noradrenergic innervation, the prefrontal cortex and the hippocampus, are particularly important with regard to these functions. Due to its role in mediating normal cognitive function, it is reasonable to expect that noradrenergic transmission becomes dysfunctional in a number of neuropsychiatric and neurodegenerative diseases characterized by cognitive deficits. In this review, we summarize the unique role that norepinephrine plays in prefrontal cortical and hippocampal function and how its interaction with its various receptors contributes to cognitive behaviors. We further assess the changes that occur in the noradrenergic system in Alzheimer’s disease, Parkinson’s disease, attention-deficit/hyperactivity disorder, and schizophrenia and how these changes contribute to cognitive decline in these pathologies. Olga Borodovitsyna, Matthew Flamini, and Daniel Chandler Copyright © 2017 Olga Borodovitsyna et al. All rights reserved. Attenuated Late-Phase Arc Transcription in the Dentate Gyrus of Mice Lacking Egr3 Mon, 15 May 2017 00:00:00 +0000 The dentate gyrus (DG) engages in sustained Arc transcription for at least 8 hours following behavioral induction, and this time course may be functionally coupled to the unique role of the DG in hippocampus-dependent learning and memory. The factors that regulate long-term DG Arc expression, however, remain poorly understood. Animals lacking Egr3 show less Arc expression following convulsive stimulation, but the effect of Egr3 ablation on behaviorally induced Arc remains unknown. To address this, Egr3−/− and wild-type (WT) mice explored novel spatial environments and were sacrificed either immediately or after 5, 60, 240, or 480 minutes, and Arc expression was quantified by fluorescence in situ hybridization. Although short-term (i.e., within 60 min) Arc expression was equivalent across genotypes, DG Arc expression was selectively reduced at 240 and 480 minutes in mice lacking Egr3. These data demonstrate the involvement of Egr3 in regulating the late protein-dependent phase of Arc expression in the DG. Amanda Maple, Rachel E. Lackie, Diana I. Elizalde, Stephanie L. Grella, Chelsey C. Damphousse, Collin Xa, Amelia L. Gallitano, and Diano F. Marrone Copyright © 2017 Amanda Maple et al. All rights reserved. Long-Term Impairment of Sound Processing in the Auditory Midbrain by Daily Short-Term Exposure to Moderate Noise Sun, 14 May 2017 10:58:05 +0000 Most citizen people are exposed daily to environmental noise at moderate levels with a short duration. The aim of the present study was to determine the effects of daily short-term exposure to moderate noise on sound level processing in the auditory midbrain. Sound processing properties of auditory midbrain neurons were recorded in anesthetized mice exposed to moderate noise (80 dB SPL, 2 h/d for 6 weeks) and were compared with those from age-matched controls. Neurons in exposed mice had a higher minimum threshold and maximum response intensity, a longer first spike latency, and a higher slope and narrower dynamic range for rate level function. However, these observed changes were greater in neurons with the best frequency within the noise exposure frequency range compared with those outside the frequency range. These sound processing properties also remained abnormal after a 12-week period of recovery in a quiet laboratory environment after completion of noise exposure. In conclusion, even daily short-term exposure to moderate noise can cause long-term impairment of sound level processing in a frequency-specific manner in auditory midbrain neurons. Liang Cheng, Shao-Hui Wang, Kang Peng, and Xiao-Mei Liao Copyright © 2017 Liang Cheng et al. All rights reserved. Biphalin, a Dimeric Enkephalin, Alleviates LPS-Induced Activation in Rat Primary Microglial Cultures in Opioid Receptor-Dependent and Receptor-Independent Manners Wed, 10 May 2017 07:39:54 +0000 Neuropathic pain is relatively less responsive to opioids than other types of pain, which is possibly due to a disrupted opioid system partially caused by the profound microglial cell activation that underlines neuroinflammation. We demonstrated that intrathecally injected biphalin, a dimeric enkephalin analog, diminished symptoms of neuropathy in a preclinical model of neuropathic pain in rats (CCI, chronic constriction injury of the sciatic nerve) at day 12 postinjury. Using primary microglial cell cultures, we revealed that biphalin did not influence cell viability but diminished NO production and expression of Iba1 in LPS-stimulated cells. Biphalin also diminished MOP receptor level, as well as pronociceptive mediators (iNOS, IL-1β, and IL-18) in an opioid receptor-dependent manner, and it was correlated with diminished p-NF-κB, p-IκB, p-p38MAPK, and TRIF levels. Biphalin reduced IL-6, IL-10, TNFα, p-STAT3, and p-ERK1/2 and upregulated SOCS3, TLR4, and MyD88; however, this effect was not reversed by naloxone pretreatment. Our study provides evidence that biphalin diminishes neuropathy symptoms, which might be partially related to reduced pronociceptive mediators released by activated microglia. Biphalin may be a putative drug for future pain therapy, especially for the treatment of neuropathic pain, when the lower analgesic effects of morphine are correlated with profound microglial cell activation. Katarzyna Popiolek-Barczyk, Anna Piotrowska, Wioletta Makuch, and Joanna Mika Copyright © 2017 Katarzyna Popiolek-Barczyk et al. All rights reserved. Sensory Eye Dominance in Treated Anisometropic Amblyopia Wed, 10 May 2017 00:00:00 +0000 Amblyopia results from inadequate visual experience during the critical period of visual development. Abnormal binocular interactions are believed to play a critical role in amblyopia. These binocular deficits can often be resolved, owing to the residual visual plasticity in amblyopes. In this study, we quantitatively measured the sensory eye dominance in treated anisometropic amblyopes to determine whether they had fully recovered. Fourteen treated anisometropic amblyopes with normal or corrected to normal visual acuity participated, and their sensory eye dominance was assessed by using a binocular phase combination paradigm. We found that the two eyes were unequal in binocular combination in most (11 out of 14) of our treated anisometropic amblyopes, but none of the controls. We concluded that the treated anisometropic amblyopes, even those with a normal range of visual acuity, exhibited abnormal binocular processing. Our results thus suggest that there is potential for improvement in treated anisometropic amblyopes that may further enhance their binocular visual functioning. Yao Chen, Jiafeng Wang, Hongmei Shi, Xiaoxiao Wang, and Lixia Feng Copyright © 2017 Yao Chen et al. All rights reserved. Right Hemisphere Grey Matter Volume and Language Functions in Stroke Aphasia Tue, 09 May 2017 09:30:29 +0000 The role of the right hemisphere (RH) in recovery from aphasia is incompletely understood. The present study quantified RH grey matter (GM) volume in individuals with chronic stroke-induced aphasia and cognitively healthy people using voxel-based morphometry. We compared group differences in GM volume in the entire RH and in RH regions-of-interest. Given that lesion site is a critical source of heterogeneity associated with poststroke language ability, we used voxel-based lesion symptom mapping (VLSM) to examine the relation between lesion site and language performance in the aphasic participants. Finally, using results derived from the VLSM as a covariate, we evaluated the relation between GM volume in the RH and language ability across domains, including comprehension and production processes both at the word and sentence levels and across spoken and written modalities. Between-subject comparisons showed that GM volume in the RH SMA was reduced in the aphasic group compared to the healthy controls. We also found that, for the aphasic group, increased RH volume in the MTG and the SMA was associated with better language comprehension and production scores, respectively. These data suggest that the RH may support functions previously performed by LH regions and have important implications for understanding poststroke reorganization. Sladjana Lukic, Elena Barbieri, Xue Wang, David Caplan, Swathi Kiran, Brenda Rapp, Todd B. Parrish, and Cynthia K. Thompson Copyright © 2017 Sladjana Lukic et al. All rights reserved. Molecular and Cellular Mechanisms of Synaptopathies Sun, 30 Apr 2017 00:00:00 +0000 Alvaro O. Ardiles, Andreas M. Grabrucker, Francisco G. Scholl, Gabby Rudenko, and Tiziana Borsello Copyright © 2017 Alvaro O. Ardiles et al. All rights reserved. Acupuncture Therapies and Neuroplasticity Thu, 27 Apr 2017 08:19:32 +0000 Cun-Zhi Liu, Jian Kong, and KeLun Wang Copyright © 2017 Cun-Zhi Liu et al. 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.