Neural Plasticity http://www.hindawi.com The latest articles from Hindawi Publishing Corporation © 2016 , Hindawi Publishing Corporation . All rights reserved. Increase in Growth Cone Size Correlates with Decrease in Neurite Growth Rate Wed, 04 May 2016 07:14:08 +0000 http://www.hindawi.com/journals/np/2016/3497901/ Several important discoveries in growth cone cell biology were made possible by the use of growth cones derived from cultured Aplysia bag cell neurons, including the characterization of the organization and dynamics of the cytoskeleton. The majority of these Aplysia studies focused on large growth cones induced by poly-L-lysine substrates at early stages in cell culture. Under these conditions, the growth cones are in a steady state with very little net advancement. Here, we offer a comprehensive cellular analysis of the motile behavior of Aplysia growth cones in culture beyond this pausing state. We found that average growth cone size decreased with cell culture time whereas average growth rate increased. This inverse correlation of growth rate and growth cone size was due to the occurrence of large growth cones with a peripheral domain larger than 100 μm2. The large pausing growth cones had central domains that were less consistently aligned with the direction of growth and could be converted into smaller, faster-growing growth cones by addition of a three-dimensional collagen gel. We conclude that the significant lateral expansion of lamellipodia and filopodia as observed during these culture conditions has a negative effect on neurite growth. Yuan Ren and Daniel M. Suter Copyright © 2016 Yuan Ren and Daniel M. Suter. All rights reserved. Transcranial Alternating Current and Random Noise Stimulation: Possible Mechanisms Tue, 03 May 2016 13:50:17 +0000 http://www.hindawi.com/journals/np/2016/3616807/ Background. Transcranial alternating current stimulation (tACS) is a relatively recent method suited to noninvasively modulate brain oscillations. Technically the method is similar but not identical to transcranial direct current stimulation (tDCS). While decades of research in animals and humans has revealed the main physiological mechanisms of tDCS, less is known about the physiological mechanisms of tACS. Method. Here, we review recent interdisciplinary research that has furthered our understanding of how tACS affects brain oscillations and by what means transcranial random noise stimulation (tRNS) that is a special form of tACS can modulate cortical functions. Results. Animal experiments have demonstrated in what way neurons react to invasively and transcranially applied alternating currents. Such findings are further supported by neural network simulations and knowledge from physics on entraining physical oscillators in the human brain. As a result, fine-grained models of the human skull and brain allow the prediction of the exact pattern of current flow during tDCS and tACS. Finally, recent studies on human physiology and behavior complete the picture of noninvasive modulation of brain oscillations. Conclusion. In future, the methods may be applicable in therapy of neurological and psychiatric disorders that are due to malfunctioning brain oscillations. Andrea Antal and Christoph S. Herrmann Copyright © 2016 Andrea Antal and Christoph S. Herrmann. All rights reserved. Synaptic Cell Adhesion Molecules in Alzheimer’s Disease Tue, 03 May 2016 13:09:55 +0000 http://www.hindawi.com/journals/np/2016/6427537/ Alzheimer’s disease (AD) is a neurodegenerative brain disorder associated with the loss of synapses between neurons in the brain. Synaptic cell adhesion molecules are cell surface glycoproteins which are expressed at the synaptic plasma membranes of neurons. These proteins play key roles in formation and maintenance of synapses and regulation of synaptic plasticity. Genetic studies and biochemical analysis of the human brain tissue, cerebrospinal fluid, and sera from AD patients indicate that levels and function of synaptic cell adhesion molecules are affected in AD. Synaptic cell adhesion molecules interact with Aβ, a peptide accumulating in AD brains, which affects their expression and synaptic localization. Synaptic cell adhesion molecules also regulate the production of Aβ via interaction with the key enzymes involved in Aβ formation. Aβ-dependent changes in synaptic adhesion affect the function and integrity of synapses suggesting that alterations in synaptic adhesion play key roles in the disruption of neuronal networks in AD. Iryna Leshchyns’ka and Vladimir Sytnyk Copyright © 2016 Iryna Leshchyns’ka and Vladimir Sytnyk. All rights reserved. Synaptic Plasticity, a Prominent Contributor to the Anxiety in Fragile X Syndrome Thu, 28 Apr 2016 17:12:27 +0000 http://www.hindawi.com/journals/np/2016/9353929/ Fragile X syndrome (FXS) is an inheritable neuropsychological disease caused by expansion of the CGG trinucleotide repeat affecting the fmr1 gene on X chromosome, resulting in silence of the fmr1 gene and failed expression of FMRP. Patients with FXS suffer from cognitive impairment, sensory integration deficits, learning disability, anxiety, autistic traits, and so forth. Specifically, the morbidity of anxiety in FXS individuals remains high from childhood to adulthood. By and large, it is common that the change of brain plasticity plays a key role in the progression of disease. But for now, most studies excessively emphasized the one-sided factor on the change of synaptic plasticity participating in the generation of anxiety during the development of FXS. Here we proposed an integrated concept to acquire better recognition about the details of this process. Tao Yang, Huan Zhao, Changbo Lu, Xiaoyu Li, Yingli Xie, Hao Fu, and Hui Xu Copyright © 2016 Tao Yang et al. All rights reserved. Mechanisms Underlying Adaptation of Respiratory Network Activity to Modulatory Stimuli in the Mouse Embryo Thu, 28 Apr 2016 13:32:41 +0000 http://www.hindawi.com/journals/np/2016/3905257/ Breathing is a rhythmic behavior that requires organized contractions of respiratory effector muscles. This behavior must adapt to constantly changing conditions in order to ensure homeostasis, proper body oxygenation, and CO2/pH regulation. Respiratory rhythmogenesis is controlled by neural networks located in the brainstem. One area considered to be essential for generating the inspiratory phase of the respiratory rhythm is the preBötzinger complex (preBötC). Rhythmogenesis emerges from this network through the interplay between the activation of intrinsic cellular properties (pacemaker properties) and intercellular synaptic connections. Respiratory activity continuously changes under the impact of numerous modulatory substances depending on organismal needs and environmental conditions. The preBötC network has been shown to become active during the last third of gestation. But only little is known regarding the modulation of inspiratory rhythmicity at embryonic stages and even less on a possible role of pacemaker neurons in this functional flexibility during the prenatal period. By combining electrophysiology and calcium imaging performed on embryonic brainstem slice preparations, we provide evidence showing that embryonic inspiratory pacemaker neurons are already intrinsically sensitive to neuromodulation and external conditions (i.e., temperature) affecting respiratory network activity, suggesting a potential role of pacemaker neurons in mediating rhythm adaptation to modulatory stimuli in the embryo. Marc Chevalier, Rafaël De Sa, Laura Cardoit, and Muriel Thoby-Brisson Copyright © 2016 Marc Chevalier et al. All rights reserved. Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress Wed, 27 Apr 2016 16:15:03 +0000 http://www.hindawi.com/journals/np/2016/7258201/ The potential contribution of inflammation to the development of neuropsychiatric diseases has recently received substantial attention. In the brain, the main immune cells are the microglia. As they are the main source of inflammatory factors, it is plausible that the regulation of their activation may be a potential therapeutic target. Fractalkine (CX3CL1) and its receptor CX3CR1 play a crucial role in the control of the biological activity of the microglia. In the present study, using microglial cultures we investigated whether fractalkine is able to reverse changes in microglia caused by a prenatal stress procedure. Our study found that the microglia do not express fractalkine. Prenatal stress decreases the expression of the fractalkine receptor, which in turn is enhanced by the administration of exogenous fractalkine. Moreover, treatment with fractalkine diminishes the prenatal stress-induced overproduction of proinflammatory factors such as IL-1β, IL-18, IL-6, TNF-α, CCL2, or NO in the microglial cells derived from prenatally stressed newborns. In conclusion, the present results revealed that the pathological activation of microglia in prenatally stressed newborns may be attenuated by fractalkine administration. Therefore, understanding of the role of the CX3CL1-CX3CR1 system may help to elucidate the mechanisms underlying the neuron-microglia interaction and its role in pathological conditions in the brain. Joanna Ślusarczyk, Ewa Trojan, Katarzyna Głombik, Katarzyna Chamera, Adam Roman, Bogusława Budziszewska, and Agnieszka Basta-Kaim Copyright © 2016 Joanna Ślusarczyk et al. All rights reserved. Differential DNA Methylation of MicroRNA Genes in Temporal Cortex from Alzheimer’s Disease Individuals Tue, 26 Apr 2016 10:24:04 +0000 http://www.hindawi.com/journals/np/2016/2584940/ This study investigated for the first time the genomewide DNA methylation changes of noncoding RNA genes in the temporal cortex samples from individuals with Alzheimer’s disease (AD). The methylome of 10 AD individuals and 10 age-matched controls were obtained using Illumina 450 K methylation array. A total of 2,095 among the 15,258 interrogated noncoding RNA CpG sites presented differential methylation, 161 of which were associated with miRNA genes. In particular, 10 miRNA CpG sites that were found to be hypermethylated in AD compared to control brains represent transcripts that have been previously associated with the disease. This miRNA set is predicted to target 33 coding genes from the neuregulin receptor complex (ErbB) signaling pathway, which is required for the neurons myelination process. For 6 of these miRNA genes (MIR9-1, MIR9-3, MIR181C, MIR124-1, MIR146B, and MIR451), the hypermethylation pattern is in agreement with previous results from literature that shows downregulation of miR-9, miR-181c, miR-124, miR-146b, and miR-451 in the AD brain. Our data implicate dysregulation of miRNA methylation as contributor to the pathogenesis of AD. Darine Villela, Rodrigo F. Ramalho, Aderbal R. T. Silva, Helena Brentani, Claudia K. Suemoto, Carlos Augusto Pasqualucci, Lea T. Grinberg, Ana C. V. Krepischi, and Carla Rosenberg Copyright © 2016 Darine Villela et al. All rights reserved. Gypenoside Attenuates β Amyloid-Induced Inflammation in N9 Microglial Cells via SOCS1 Signaling Tue, 26 Apr 2016 09:22:17 +0000 http://www.hindawi.com/journals/np/2016/6362707/ Reducing β amyloid- (Aβ-) induced microglial activation is believed to be effective in treating Alzheimer’s disease (AD). Microglia can be activated into classic activated state (M1 state) or alternative activated state (M2 state), and the former is harmful; in contrast, the latter is beneficial. Gypenoside (GP) is the major bioactive constituent of Gynostemma pentaphyllum, a traditional Chinese herb medicine. In this study, we hypothesized that GP attenuates Aβ-induced microglial activation by ameliorating microglial M1/M2 states, and the process may be mediated by suppressor of cell signaling protein 1 (SOCS1). In this study, we found that Aβ exposure increased the levels of microglial M1 markers, including iNOS expression, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 releases, and coadministration of GP reversed the increase of M1 markers and enhanced the levels of M2 markers, including arginase-1 (Arg-1) expression, IL-10, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF) releases in the Aβ-treated microglial cells. SOCS1-siRNA, however, significantly abolished the GP-induced effects on the levels of microglial M1 and M2 markers. These findings indicated that GP attenuates Aβ-induced microglial activation by ameliorating M1/M2 states, and the process may be mediated by SOCS1. Hui Cai, Qianlei Liang, and Guanqun Ge Copyright © 2016 Hui Cai et al. All rights reserved. Neural Correlates of Dual-Task Walking: Effects of Cognitive versus Motor Interference in Young Adults Wed, 20 Apr 2016 14:27:46 +0000 http://www.hindawi.com/journals/np/2016/8032180/ Walking while concurrently performing cognitive and/or motor interference tasks is the norm rather than the exception during everyday life and there is evidence from behavioral studies that it negatively affects human locomotion. However, there is hardly any information available regarding the underlying neural correlates of single- and dual-task walking. We had 12 young adults (23.8 ± 2.8 years) walk while concurrently performing a cognitive interference (CI) or a motor interference (MI) task. Simultaneously, neural activation in frontal, central, and parietal brain areas was registered using a mobile EEG system. Results showed that the MI task but not the CI task affected walking performance in terms of significantly decreased gait velocity and stride length and significantly increased stride time and tempo-spatial variability. Average activity in alpha and beta frequencies was significantly modulated during both CI and MI walking conditions in frontal and central brain regions, indicating an increased cognitive load during dual-task walking. Our results suggest that impaired motor performance during dual-task walking is mirrored in neural activation patterns of the brain. This finding is in line with established cognitive theories arguing that dual-task situations overstrain cognitive capabilities resulting in motor performance decrements. Rainer Beurskens, Fabian Steinberg, Franziska Antoniewicz, Wanja Wolff, and Urs Granacher Copyright © 2016 Rainer Beurskens et al. All rights reserved. Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study Mon, 18 Apr 2016 12:31:32 +0000 http://www.hindawi.com/journals/np/2016/7607924/ Glutamatergic gliotransmission, that is, the release of glutamate from perisynaptic astrocyte processes in an activity-dependent manner, has emerged as a potentially crucial signaling pathway for regulation of synaptic plasticity, yet its modes of expression and function in vivo remain unclear. Here, we focus on two experimentally well-identified gliotransmitter pathways, (i) modulations of synaptic release and (ii) postsynaptic slow inward currents mediated by glutamate released from astrocytes, and investigate their possible functional relevance on synaptic plasticity in a biophysical model of an astrocyte-regulated synapse. Our model predicts that both pathways could profoundly affect both short- and long-term plasticity. In particular, activity-dependent glutamate release from astrocytes could dramatically change spike-timing-dependent plasticity, turning potentiation into depression (and vice versa) for the same induction protocol. Maurizio De Pittà and Nicolas Brunel Copyright © 2016 Maurizio De Pittà and Nicolas Brunel. All rights reserved. Form and Function of Sleep Spindles across the Lifespan Thu, 14 Apr 2016 14:09:45 +0000 http://www.hindawi.com/journals/np/2016/6936381/ Since the advent of EEG recordings, sleep spindles have been identified as hallmarks of non-REM sleep. Despite a broad general understanding of mechanisms of spindle generation gleaned from animal studies, the mechanisms underlying certain features of spindles in the human brain, such as “global” versus “local” spindles, are largely unknown. Neither the topography nor the morphology of sleep spindles remains constant throughout the lifespan. It is likely that changes in spindle phenomenology during development and aging are the result of dramatic changes in brain structure and function. Across various developmental windows, spindle activity is correlated with general cognitive aptitude, learning, and memory; however, these correlations vary in strength, and even direction, depending on age and metrics used. Understanding these differences across the lifespan should further clarify how these oscillations are generated and their function under a variety of circumstances. We discuss these issues, and their translational implications for human cognitive function. Because sleep spindles are similarly affected in disorders of neurodevelopment (such as schizophrenia) and during aging (such as neurodegenerative conditions), both types of disorders may benefit from therapies based on a better understanding of spindle function. Brittany C. Clawson, Jaclyn Durkin, and Sara J. Aton Copyright © 2016 Brittany C. Clawson et al. All rights reserved. Role of Striatal-Enriched Tyrosine Phosphatase in Neuronal Function Tue, 12 Apr 2016 16:11:46 +0000 http://www.hindawi.com/journals/np/2016/8136925/ Striatal-enriched protein tyrosine phosphatase (STEP) is a CNS-enriched protein implicated in multiple neurologic and neuropsychiatric disorders. STEP regulates key signaling proteins required for synaptic strengthening as well as NMDA and AMPA receptor trafficking. Both high and low levels of STEP disrupt synaptic function and contribute to learning and behavioral deficits. High levels of STEP are present in human postmortem samples and animal models of Alzheimer’s disease, Parkinson’s disease, and schizophrenia and in animal models of fragile X syndrome. Low levels of STEP activity are present in additional disorders that include ischemia, Huntington’s chorea, alcohol abuse, and stress disorders. Thus the current model of STEP is that optimal levels are required for optimal synaptic function. Here we focus on the role of STEP in Alzheimer’s disease and the mechanisms by which STEP activity is increased in this illness. Both genetic lowering of STEP levels and pharmacological inhibition of STEP activity in mouse models of Alzheimer’s disease reverse the biochemical and cognitive abnormalities that are present. These findings suggest that STEP is an important point for modulation of proteins required for synaptic plasticity. Marija Kamceva, Jessie Benedict, Angus C. Nairn, and Paul J. Lombroso Copyright © 2016 Marija Kamceva et al. All rights reserved. The Contribution of Thalamocortical Core and Matrix Pathways to Sleep Spindles Sun, 10 Apr 2016 11:15:52 +0000 http://www.hindawi.com/journals/np/2016/3024342/ Sleep spindles arise from the interaction of thalamic and cortical neurons. Neurons in the thalamic reticular nucleus (TRN) inhibit thalamocortical neurons, which in turn excite the TRN and cortical neurons. A fundamental principle of anatomical organization of the thalamocortical projections is the presence of two pathways: the diffuse matrix pathway and the spatially selective core pathway. Cortical layers are differentially targeted by these two pathways with matrix projections synapsing in superficial layers and core projections impinging on middle layers. Based on this anatomical observation, we propose that spindles can be classified into two classes, those arising from the core pathway and those arising from the matrix pathway, although this does not exclude the fact that some spindles might combine both pathways at the same time. We find evidence for this hypothesis in EEG/MEG studies, intracranial recordings, and computational models that incorporate this difference. This distinction will prove useful in accounting for the multiple functions attributed to spindles, in that spindles of different types might act on local and widespread spatial scales. Because spindle mechanisms are often hijacked in epilepsy and schizophrenia, the classification proposed in this review might provide valuable information in defining which pathways have gone awry in these neurological disorders. Giovanni Piantoni, Eric Halgren, and Sydney S. Cash Copyright © 2016 Giovanni Piantoni et al. All rights reserved. Age-Related Effects on Future Mental Time Travel Thu, 07 Apr 2016 14:09:50 +0000 http://www.hindawi.com/journals/np/2016/1867270/ Mental time travel (MTT), the ability to travel mentally back and forward in time in order to reexperience past events and preexperience future events, is crucial in human cognition. As we move along life, MTT may be changed accordingly. However, the relation between re- and preexperiencing along the lifespan is still not clear. Here, young and older adults underwent a psychophysical paradigm assessing two different components of MTT: self-projection, which is the ability to project the self towards a past or a future location of the mental time line, and self-reference, which is the ability to determine whether events are located in the past or future in reference to that given self-location. Aged individuals performed worse in both self-projection to the future and self-reference to future events compared to young individuals. In addition, aging decreased older adults’ preference for personal compared to nonpersonal events. These results demonstrate the impact of MTT and self-processing on subjective time processing in healthy aging. Changes in memory functions in aged people may therefore be related not only to memory per se, but also to the relations of memory and self. Filomena Anelli, Elisa Ciaramelli, Shahar Arzy, and Francesca Frassinetti Copyright © 2016 Filomena Anelli et al. All rights reserved. Neural Plasticity in Obesity and Psychiatric Disorders Thu, 07 Apr 2016 06:47:15 +0000 http://www.hindawi.com/journals/np/2016/6053871/ Mauricio Arcos-Burgos, Maria T. Acosta, Ariel F. Martinez, Maximilian Muenke, Pablo J. Enriori, and Claudio A. Mastronardi Copyright © 2016 Mauricio Arcos-Burgos et al. All rights reserved. Plastic Change along the Intact Crossed Pathway in Acute Phase of Cerebral Ischemia Revealed by Optical Intrinsic Signal Imaging Wed, 06 Apr 2016 07:49:24 +0000 http://www.hindawi.com/journals/np/2016/1923160/ The intact crossed pathway via which the contralesional hemisphere responds to the ipsilesional somatosensory input has shown to be affected by unilateral stroke. The aim of this study was to investigate the plasticity of the intact crossed pathway in response to different intensities of stimulation in a rodent photothrombotic stroke model. Using optical intrinsic signal imaging, an overall increase of the contralesional cortical response was observed in the acute phase (≤48 hours) after stroke. In particular, the contralesional hyperactivation is more prominent under weak stimulations, while a strong stimulation would even elicit a depressed response. The results suggest a distinct stimulation-response pattern along the intact crossed pathway after stroke. We speculate that the contralesional hyperactivation under weak stimulations was due to the reorganization for compensatory response to the weak ipsilateral somatosensory input. Xiaoli Guo, Yongzhi He, Hongyang Lu, Yao Li, Xin Su, Ying Jiang, and Shanbao Tong Copyright © 2016 Xiaoli Guo et al. All rights reserved. Regulation of the Postsynaptic Compartment of Excitatory Synapses by the Actin Cytoskeleton in Health and Its Disruption in Disease Tue, 05 Apr 2016 13:30:50 +0000 http://www.hindawi.com/journals/np/2016/2371970/ Disruption of synaptic function at excitatory synapses is one of the earliest pathological changes seen in wide range of neurological diseases. The proper control of the segregation of neurotransmitter receptors at these synapses is directly correlated with the intact regulation of the postsynaptic cytoskeleton. In this review, we are discussing key factors that regulate the structure and dynamics of the actin cytoskeleton, the major cytoskeletal building block that supports the postsynaptic compartment. Special attention is given to the complex interplay of actin-associated proteins that are found in the synaptic specialization. We then discuss our current understanding of how disruption of these cytoskeletal elements may contribute to the pathological events observed in the nervous system under disease conditions with a particular focus on Alzheimer’s disease pathology. Holly Stefen, Chanchanok Chaichim, John Power, and Thomas Fath Copyright © 2016 Holly Stefen et al. All rights reserved. Seizure-Induced Regulations of Amyloid-β, STEP61, and STEP61 Substrates Involved in Hippocampal Synaptic Plasticity Tue, 05 Apr 2016 11:39:19 +0000 http://www.hindawi.com/journals/np/2016/2123748/ Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline. Pathologic accumulation of soluble amyloid-β (Aβ) oligomers impairs synaptic plasticity and causes epileptic seizures, both of which contribute to cognitive dysfunction in AD. However, whether seizures could regulate Aβ-induced synaptic weakening remains unclear. Here we show that a single episode of electroconvulsive seizures (ECS) increased protein expression of membrane-associated STriatal-Enriched protein tyrosine Phosphatase (STEP61) and decreased tyrosine-phosphorylation of its substrates N-methyl D-aspartate receptor (NMDAR) subunit GluN2B and extracellular signal regulated kinase 1/2 (ERK1/2) in the rat hippocampus at 2 days following a single ECS. Interestingly, a significant decrease in ERK1/2 expression and an increase in APP and Aβ levels were observed at 3-4 days following a single ECS when STEP61 level returned to the baseline. Given that pathologic levels of Aβ increase STEP61 activity and STEP61-mediated dephosphorylation of GluN2B and ERK1/2 leads to NMDAR internalization and ERK1/2 inactivation, we propose that upregulation of STEP61 and downregulation of GluN2B and ERK1/2 phosphorylation mediate compensatory weakening of synaptic strength in response to acute enhancement of hippocampal network activity, whereas delayed decrease in ERK1/2 expression and increase in APP and Aβ expression may contribute to the maintenance of this synaptic weakening. Sung-Soo Jang, Sara E. Royston, Gunhee Lee, Shuwei Wang, and Hee Jung Chung Copyright © 2016 Sung-Soo Jang et al. All rights reserved. Promoting Motor Cortical Plasticity with Acute Aerobic Exercise: A Role for Cerebellar Circuits Mon, 04 Apr 2016 09:17:38 +0000 http://www.hindawi.com/journals/np/2016/6797928/ Acute aerobic exercise facilitated long-term potentiation-like plasticity in the human primary motor cortex (M1). Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age: years). In Experiment   1, acute aerobic exercise reduced cerebellar inhibition (CBI) (, ), elicited by dual-coil paired-pulse transcranial magnetic stimulation. In Experiment   2, we evaluated the facilitatory effects of aerobic exercise on responses to paired associative stimulation, delivered with a 25 ms (PAS25) or 21 ms (PAS21) interstimulus interval ( per group). Increased M1 excitability evoked by PAS25, but not PAS21, relies on trans-cerebellar sensory pathways. The magnitude of the aerobic exercise effect on PAS response was not significantly different between PAS protocols (interaction effect: ); however, planned comparisons indicated that, relative to a period of rest, acute aerobic exercise enhanced the excitatory response to PAS25 (), but not PAS21 (). Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity. The findings have implications for developing aerobic exercise strategies to “prime” M1 plasticity for enhanced motor skill learning in applied settings. Cameron S. Mang, Katlyn E. Brown, Jason L. Neva, Nicholas J. Snow, Kristin L. Campbell, and Lara A. Boyd Copyright © 2016 Cameron S. Mang et al. All rights reserved. Molecular Mechanisms of Dendritic Spine Development and Plasticity Sun, 03 Apr 2016 11:15:27 +0000 http://www.hindawi.com/journals/np/2016/2078121/ Kwok-On Lai, Bryen A. Jordan, Xin-Ming Ma, Deepak P. Srivastava, and Kimberly F. Tolias Copyright © 2016 Kwok-On Lai et al. All rights reserved. The Case of the Disappearing Spindle Burst Mon, 28 Mar 2016 14:16:58 +0000 http://www.hindawi.com/journals/np/2016/8037321/ Sleep spindles are brief cortical oscillations at 10–15 Hz that occur predominantly during non-REM (quiet) sleep in adult mammals and are thought to contribute to learning and memory. Spindle bursts are phenomenologically similar to sleep spindles, but they occur predominantly in early infancy and are triggered by peripheral sensory activity (e.g., by retinal waves); accordingly, spindle bursts are thought to organize neural networks in the developing brain and establish functional links with the sensory periphery. Whereas the spontaneous retinal waves that trigger spindle bursts in visual cortex are a transient feature of early development, the myoclonic twitches that drive spindle bursts in sensorimotor cortex persist into adulthood. Moreover, twitches—and their associated spindle bursts—occur exclusively during REM (active) sleep. Curiously, despite the persistence of twitching into adulthood, twitch-related spindle bursts have not been reported in adult sensorimotor cortex. This raises the question of whether such spindle burst activity does not occur in adulthood or, alternatively, occurs but has yet to be discovered. If twitch-related spindle bursts do occur in adults, they could contribute to the calibration, maintenance, and repair of sensorimotor systems. Alexandre Tiriac and Mark S. Blumberg Copyright © 2016 Alexandre Tiriac and Mark S. Blumberg. All rights reserved. Sleep Spindles as Facilitators of Memory Formation and Learning Mon, 28 Mar 2016 11:26:46 +0000 http://www.hindawi.com/journals/np/2016/1796715/ Over the past decades important progress has been made in understanding the mechanisms of sleep spindle generation. At the same time a physiological role of sleep spindles is starting to be revealed. Behavioural studies in humans and animals have found significant correlations between the recall performance in different learning tasks and the amount of sleep spindles in the intervening sleep. Concomitant neurophysiological experiments showed a close relationship between sleep spindles and other sleep related EEG rhythms as well as a relationship between sleep spindles and synaptic plasticity. Together, there is growing evidence from several disciplines in neuroscience for a participation of sleep spindles in memory formation and learning. Daniel Ulrich Copyright © 2016 Daniel Ulrich. All rights reserved. Neural Plasticity and Neurogenesis in Mental Disorders Mon, 28 Mar 2016 08:37:54 +0000 http://www.hindawi.com/journals/np/2016/3738015/ Graham Cocks, Mauro G. Carta, Oscar Arias-Carrión, and Antonio E. Nardi Copyright © 2016 Graham Cocks et al. All rights reserved. Brain Network Architecture and Plasticity: MR Neuroimaging Perspectives Sun, 27 Mar 2016 11:25:48 +0000 http://www.hindawi.com/journals/np/2016/6952169/ Feng Shi, Yong Liu, Shuyu Li, Xiaobo Li, and Martin Walter Copyright © 2016 Feng Shi et al. All rights reserved. Developmental Changes in Sleep Spindle Characteristics and Sigma Power across Early Childhood Sun, 27 Mar 2016 07:51:52 +0000 http://www.hindawi.com/journals/np/2016/3670951/ Sleep spindles, a prominent feature of the non-rapid eye movement (NREM) sleep electroencephalogram (EEG), are linked to cognitive abilities. Early childhood is a time of rapid cognitive and neurophysiological maturation; however, little is known about developmental changes in sleep spindles. In this study, we longitudinally examined trajectories of multiple sleep spindle characteristics (i.e., spindle duration, frequency, integrated spindle amplitude, and density) and power in the sigma frequency range (10–16 Hz) across ages 2, 3, and 5 years (; 3 males). At each time point, nocturnal sleep EEG was recorded in-home after 13-h of prior wakefulness. Spindle duration, integrated spindle amplitude, and sigma power increased with age across all EEG derivations (C3A2, C4A1, O2A1, and O1A2; all s < 0.05). We also found a developmental decrease in mean spindle frequency () but no change in spindle density with increasing age. Thus, sleep spindles increased in duration and amplitude but decreased in frequency across early childhood. Our data characterize early developmental changes in sleep spindles, which may advance understanding of thalamocortical brain connectivity and associated lifelong disease processes. These findings also provide unique insights into spindle ontogenesis in early childhood and may help identify electrophysiological features related to healthy and aberrant brain maturation. Ian J. McClain, Caroline Lustenberger, Peter Achermann, Jonathan M. Lassonde, Salome Kurth, and Monique K. LeBourgeois Copyright © 2016 Ian J. McClain et al. All rights reserved. Effects of Chronic Dopamine D2R Agonist Treatment and Polysialic Acid Depletion on Dendritic Spine Density and Excitatory Neurotransmission in the mPFC of Adult Rats Wed, 23 Mar 2016 12:16:22 +0000 http://www.hindawi.com/journals/np/2016/1615363/ Dopamine D2 receptors (D2R) in the medial prefrontal cortex (mPFC) are key players in the etiology and therapeutics of schizophrenia. The overactivation of these receptors contributes to mPFC dysfunction. Chronic treatment with D2R agonists modifies the expression of molecules implicated in neuronal structural plasticity, synaptic function, and inhibitory neurotransmission, which are also altered in schizophrenia. These changes are dependent on the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a plasticity-related molecule, but nothing is known about the effects of D2R and PSA-NCAM on excitatory neurotransmission and the structure of mPFC pyramidal neurons, two additional features affected in schizophrenia. To evaluate these parameters, we have chronically treated adult rats with PPHT (a D2R agonist) after enzymatic removal of PSA with Endo-N. Both treatments decreased spine density in apical dendrites of pyramidal neurons without affecting their inhibitory innervation. Endo-N also reduced the expression of vesicular glutamate transporter-1. These results indicate that D2R and PSA-NCAM are important players in the regulation of the structural plasticity of mPFC excitatory neurons. This is relevant to our understanding of the neurobiological basis of schizophrenia, in which structural alterations of pyramidal neurons and altered expression of D2R and PSA-NCAM have been found. Esther Castillo-Gómez, Emilio Varea, José Miguel Blasco-Ibáñez, Carlos Crespo, and Juan Nacher Copyright © 2016 Esther Castillo-Gómez et al. All rights reserved. Connecting Synaptic Activity with Plasticity-Related Gene Expression: From Molecular Mechanisms to Neurological Disorders Sun, 20 Mar 2016 13:23:02 +0000 http://www.hindawi.com/journals/np/2016/7149527/ Pablo Muñoz, Armaz Aschrafi, and Pablo R. Moya Copyright © 2016 Pablo Muñoz et al. All rights reserved. The Many Faces of Stress: Implications for Neuropsychiatric Disorders Thu, 17 Mar 2016 10:02:04 +0000 http://www.hindawi.com/journals/np/2016/8389737/ Laura Musazzi and Jordan Marrocco Copyright © 2016 Laura Musazzi and Jordan Marrocco. All rights reserved. The Neural Correlates of Long-Term Carryover following Functional Electrical Stimulation for Stroke Thu, 17 Mar 2016 07:50:29 +0000 http://www.hindawi.com/journals/np/2016/4192718/ Neurorehabilitation effective delivery for stroke is likely to be improved by establishing a mechanistic understanding of how to enhance adaptive plasticity. Functional electrical stimulation is effective at reducing poststroke foot drop; in some patients, the effect persists after therapy has finished with an unknown mechanism. We used fMRI to examine neural correlates of functional electrical stimulation key elements, volitional intent to move and concurrent stimulation, in a group of chronic stroke patients receiving functional electrical stimulation for foot-drop correction. Patients exhibited task-related activation in a complex network, sharing bilateral sensorimotor and supplementary motor activation with age-matched controls. We observed consistent separation of patients with and without carryover effect on the basis of brain responses. Patients who experienced the carryover effect had responses in supplementary motor area that correspond to healthy controls; the interaction between experimental factors in contralateral angular gyrus was seen only in those without carryover. We suggest that the functional electrical stimulation carryover mechanism of action is based on movement prediction and sense of agency/body ownership—the ability of a patient to plan the movement and to perceive the stimulation as a part of his/her own control loop is important for carryover effect to take place. Marta Gandolla, Nick S. Ward, Franco Molteni, Eleonora Guanziroli, Giancarlo Ferrigno, and Alessandra Pedrocchi Copyright © 2016 Marta Gandolla et al. All rights reserved. Amyloid-β-Induced Dysregulation of AMPA Receptor Trafficking Thu, 17 Mar 2016 06:43:49 +0000 http://www.hindawi.com/journals/np/2016/3204519/ Evidence from neuropathological, genetic, animal model, and biochemical studies has indicated that the accumulation of amyloid-beta (Aβ) is associated with, and probably induces, profound neuronal changes in brain regions critical for memory and cognition in the development of Alzheimer’s disease (AD). There is considerable evidence that synapses are particularly vulnerable to AD, establishing synaptic dysfunction as one of the earliest events in pathogenesis, prior to neuronal loss. It is clear that excessive Aβ levels can disrupt excitatory synaptic transmission and plasticity, mainly due to dysregulation of the AMPA and NMDA glutamate receptors in the brain. Importantly, AMPA receptors are the principal glutamate receptors that mediate fast excitatory neurotransmission. This is essential for synaptic plasticity, a cellular correlate of learning and memory, which are the cognitive functions that are most disrupted in AD. Here we review recent advances in the field and provide insights into the molecular mechanisms that underlie Aβ-induced dysfunction of AMPA receptor trafficking. This review focuses primarily on NMDA receptor- and metabotropic glutamate receptor-mediated signaling. In particular, we highlight several mechanisms that underlie synaptic long-term depression as common signaling pathways that are hijacked by the neurotoxic effects of Aβ. Sumasri Guntupalli, Jocelyn Widagdo, and Victor Anggono Copyright © 2016 Sumasri Guntupalli et al. All rights reserved.