http://www.hindawi.com The latest articles from Hindawi Publishing Corporation © 2013 , Hindawi Publishing Corporation . All rights reserved. Sun, 19 May 2013 10:15:22 +0000 http://www.hindawi.com/journals/np/2013/176183/ Matteo Caleo, Giorgio M. Innocenti, and Maurice Ptito Copyright © 2013 Matteo Caleo et al. All rights reserved. Thu, 02 May 2013 10:04:58 +0000 http://www.hindawi.com/journals/np/2013/653572/ We report the first neural recording during ecstatic meditations called jhanas and test whether a brain reward system plays a role in the joy reported. Jhanas are Altered States of Consciousness (ASC) that imply major brain changes based on subjective reports: (1) external awareness dims, (2) internal verbalizations fade, (3) the sense of personal boundaries is altered, (4) attention is highly focused on the object of meditation, and (5) joy increases to high levels. The fMRI and EEG results from an experienced meditator show changes in brain activity in 11 regions shown to be associated with the subjective reports, and these changes occur promptly after jhana is entered. In particular, the extreme joy is associated not only with activation of cortical processes but also with activation of the nucleus accumbens (NAc) in the dopamine/opioid reward system. We test three mechanisms by which the subject might stimulate his own reward system by external means and reject all three. Taken together, these results demonstrate an apparently novel method of self-stimulating a brain reward system using only internal mental processes in a highly trained subject. Michael R. Hagerty, Julian Isaacs, Leigh Brasington, Larry Shupe, Eberhard E. Fetz, and Steven C. Cramer Copyright © 2013 Michael R. Hagerty et al. All rights reserved. Mon, 29 Apr 2013 14:49:35 +0000 http://www.hindawi.com/journals/np/2013/263287/ The aim of the present study is to detect a combination method to utilize gene therapy for the treatment of Parkinson‘s disease (PD). Here, a PD rat model is used for the in vivo gene therapy of a recombinant adeno-associated virus (AAV2) containing a human glutamic acid decarboxylase 65 (rAAV2-hGAD65) gene delivered to the subthalamic nucleus (STN). This is combined with the ex vivo gene delivery of tyrosine hydroxylase (TH) by fibroblasts injected into the striatum. After the treatment, the rotation behavior was improved with the greatest efficacy in the combination group. The results of immunohistochemistry showed that hGAD65 gene delivery by AAV2 successfully led to phenotypic changes of neurons in STN. And the levels of glutamic acid and GABA in the internal segment of the globus pallidus (GPi) and substantia nigra pars reticulata (SNr) were obviously lower than the control groups. However, hGAD65 gene transfer did not effectively protect surviving dopaminergic neurons in the SNc and VTA. This study suggests that subthalamic hGAD65 gene therapy and combined with TH gene therapy can alleviate symptoms of the PD model rats, independent of the protection the DA neurons from death. Deyu Zheng, Xiaohua Jiang, Junpeng Zhao, Deyi Duan, Huanying Zhao, and Qunyuan Xu Copyright © 2013 Deyu Zheng et al. All rights reserved. Wed, 24 Apr 2013 14:25:35 +0000 http://www.hindawi.com/journals/np/2013/924192/ The motor function is controlled by the motor system that comprises a series of cortical and subcortical areas interacting via anatomical connections. The motor function will be disturbed when the stroke lesion impairs either any of these areas or their connections. More and more evidence indicates that the reorganization of the motor network including both areas and their anatomical and functional connectivity might contribute to the motor recovery after stroke. Here, we review recent studies employing models of anatomical, functional, and effective connectivity on neuroimaging data to investigate how ischemic stroke influences the connectivity of motor areas and how changes in connectivity relate to impaired function and functional recovery. We suggest that connectivity changes constitute an important pathophysiological aspect of motor impairment after stroke and important mechanisms of motor recovery. We also demonstrate that therapeutic interventions may facilitate motor recovery after stroke by modulating the connectivity among the motor areas. In conclusion, connectivity analyses improved our understanding of the mechanisms of motor recovery after stroke and may help to design hypothesis-driven treatment strategies and sensitive measures for outcome prediction in stroke patients. Lin Jiang, Huijuan Xu, and Chunshui Yu Copyright © 2013 Lin Jiang et al. All rights reserved. Thu, 18 Apr 2013 17:33:01 +0000 http://www.hindawi.com/journals/np/2013/128236/ The blind subjects have experienced a series of brain structural and functional alterations due to the visual deprivation. It remains unclear as to whether white matter changes differ between blind subjects with visual deprivation before and after a critical developmental period. The present study offered a direct comparison in changes of white matter fractional anisotropy (FA) between congenital blind (CB) and late blind (LB) individuals. Twenty CB, 21 LB (blindness onset after 18 years old), and 40 sight control (SC) subjects were recruited. Both the tract-based spatial statistics (TBSS) and voxel-based analysis (VBA) showed lower FA in the bilateral optic radiations in both blind groups, suggesting that the loss of white matter integrity was the prominent hallmark in the blind people. The LB group showed more extensive white matter impairment than the CB group, indicating the mechanisms of white matter FA changes are different between the CB and LB groups. Using a loose threshold, a trend of an increased FA was found in the bilateral corticospinal tracts in the LB but with a smaller spatial extent relative to the CB. These results suggest that white matter FA changes in the blind subjects are the reflection of multiple mechanisms, including the axonal degeneration, deafferentation, and plasticity. Dawei Wang, Wen Qin, Yong Liu, Yunting Zhang, Tianzi Jiang, and Chunshui Yu Copyright © 2013 Dawei Wang et al. All rights reserved. Sun, 14 Apr 2013 14:39:01 +0000 http://www.hindawi.com/journals/np/2013/698528/ Brain cancer is a common type of childhood malignancy, and radiotherapy (RT) is a mainstay of treatment. RT is effective for tumor eradication, and survival rates are high. However, RT damages the brain and disrupts ongoing developmental processes, resulting in debilitating cognitive “late” effects that may take years to fully manifest. These late effects likely derive from a long-term decrement in cell proliferation, combined with a neural environment that is hostile to plasticity, both of which are induced by RT. Long-term suppression of cell proliferation deprives the brain of the raw materials needed for optimum cognitive performance (such as new neurons in the hippocampus and new glia in frontal cortex), while chronic inflammation and dearth of trophic substances (such as growth hormone) limit neuroplastic potential in existing circuitry. Potential treatments for cognitive late effects should address both of these conditions. Exercise represents one such potential treatment, since it has the capacity to enhance cell proliferation, as well as to promote a neural milieu permissive for plasticity. Here, we review the evidence that cognitive late effects can be traced to RT-induced suppression of cell proliferation and hostile environmental conditions, as well as emerging evidence that exercise may be effective as an independent or adjuvant therapy. Shaefali P. Rodgers, Melissa Trevino, Janice A. Zawaski, M. Waleed Gaber, and J. Leigh Leasure Copyright © 2013 Shaefali P. Rodgers et al. All rights reserved. Tue, 09 Apr 2013 09:53:50 +0000 http://www.hindawi.com/journals/np/2013/805497/ Depression is a devastating and prevalent disease, with profound effects on neural structure and function; however the etiology and neuropathology of depression remain poorly understood. Though antidepressant drugs exist, they are not ideal, as only a segment of patients are effectively treated, therapeutic onset is delayed, and the exact mechanism of these drugs remains to be elucidated. Several theories of depression do exist, including modulation of monoaminergic neurotransmission, alterations in neurotrophic factors, and the upregulation of adult hippocampal neurogenesis, and are briefly mentioned in the review. However none of these theories sufficiently explains the pathology and treatment of depression unto itself. Recently, neural plasticity theories of depression have postulated that multiple aspects of brain plasticity, beyond neurogenesis, may bridge the prevailing theories. The term “neural plasticity” encompasses an array of mechanisms, from the birth, survival, migration, and integration of new neurons to neurite outgrowth, synaptogenesis, and the modulation of mature synapses. This review critically assesses the role of adult hippocampal neurogenesis and the cell adhesion molecule, PSA-NCAM (which is known to be involved in many facets of neural plasticity), in depression and antidepressant treatment. Steven R. Wainwright and Liisa A. M. Galea Copyright © 2013 Steven R. Wainwright and Liisa A. M. Galea. All rights reserved. Sun, 31 Mar 2013 12:21:56 +0000 http://www.hindawi.com/journals/np/2013/971817/ A growing body of evidence suggests that psychological stress is a major risk factor for psychiatric disorders. The basic mechanisms are still under investigation but involve changes in neuroendocrine-immune interactions, ultimately affecting brain plasticity. In this study we characterized central and peripheral effects of different stressors, applied for different time lengths, in adult male C57BL/6J mice. We compared the effects of repeated (7 versus 21 days) restraint stress (RS) and chronic disruption of social hierarchy (SS) on neuroendocrine (corticosterone) and immune function (cytokines and splenic apoptosis) and on a marker of brain plasticity (brain-derived neurotrophic factor, BDNF ). Neuroendocrine activation did not differ between SS and control subjects; by contrast, the RS group showed a strong neuroendocrine response characterized by a specific time-dependent profile. Immune function and hippocampal BDNF levels were inversely related to hypothalamic-pituitary-adrenal axis activation. These data show a fine modulation of the crosstalk between central and peripheral pathways of adaptation and plasticity and suggest that the length of stress exposure is crucial to determine its final outcome on health or disease. Sara Capoccia, Alessandra Berry, Veronica Bellisario, Davide Vacirca, Elena Ortona, Enrico Alleva, and Francesca Cirulli Copyright © 2013 Sara Capoccia et al. All rights reserved. Sun, 24 Mar 2013 19:07:41 +0000 http://www.hindawi.com/journals/np/2013/397176/ Recent work about the role of visual callosal connections in ferrets and cats is reviewed, and morphological and functional homologies between the lateral intrinsic and callosal network in early visual areas are discussed. Both networks selectively link distributed neuronal groups with similar response properties, and the actions exerted by callosal input reflect the functional topography of those networks. This supports the notion that callosal connections perpetuate the function of the lateral intrahemispheric circuit onto the other hemisphere. Reversible deactivation studies indicate that the main action of visual callosal input is a multiplicative shift of responses rather than a changing response selectivity. Both the gain of that action and its excitatory-inhibitory balance seem to be dynamically adapted to the feedforward drive by the visual stimulus onto primary visual cortex. Taken together anatomical and functional evidence from corticocortical and lateral circuits further leads to the conclusion that visual callosal connections share more features with lateral intrahemispheric connections on the same hierarchical level and less with feedback connections. I propose that experimental results about the callosal circuit in early visual areas can be interpreted with respect to lateral connectivity in general. Kerstin E. Schmidt Copyright © 2013 Kerstin E. Schmidt. All rights reserved. Mon, 18 Mar 2013 11:49:32 +0000 http://www.hindawi.com/journals/np/2013/603502/ Transcranial direct current stimulation (tDCS) is a noninvasive technique that modulates the excitability of neurons within the motor cortex (M1). Although the aftereffects of anodal tDCS on modulating cortical excitability have been described, there is limited data describing the outcomes of different tDCS intensities on intracortical circuits. To further elucidate the mechanisms underlying the aftereffects of M1 excitability following anodal tDCS, we used transcranial magnetic stimulation (TMS) to examine the effect of different intensities on cortical excitability and short-interval intracortical inhibition (SICI). Using a randomized, counterbalanced, crossover design, with a one-week wash-out period, 14 participants (6 females and 8 males, 22–45 years) were exposed to 10 minutes of anodal tDCS at 0.8, 1.0, and 1.2 mA. TMS was used to measure M1 excitability and SICI of the contralateral wrist extensor muscle at baseline, immediately after and 15 and 30 minutes following cessation of anodal tDCS. Cortical excitability increased, whilst SICI was reduced at all time points following anodal tDCS. Interestingly, there were no differences between the three intensities of anodal tDCS on modulating cortical excitability or SICI. These results suggest that the aftereffect of anodal tDCS on facilitating cortical excitability is due to the modulation of synaptic mechanisms associated with long-term potentiation and is not influenced by different tDCS intensities. Dawson J. Kidgell, Robin M. Daly, Kayleigh Young, Jarrod Lum, Gregory Tooley, Shapour Jaberzadeh, Maryam Zoghi, and Alan J. Pearce Copyright © 2013 Dawson J. Kidgell et al. All rights reserved. Thu, 14 Mar 2013 10:57:39 +0000 http://www.hindawi.com/journals/np/2013/396865/ Repetitive performance of a task can result in learning. The neural mechanisms underpinning such use-dependent plasticity are influenced by several neuromodulators. Variations in neuromodulator levels may contribute to the variability in performance outcomes following training. Circulating levels of the neuromodulator cortisol change throughout the day. High cortisol levels inhibit neuroplasticity induced with a transcranial magnetic stimulation (TMS) paradigm that has similarities to use-dependent plasticity. The present study investigated whether performance changes following a motor training task are modulated by time of day and/or changes in endogenous cortisol levels. Motor training involving 30 minutes of repeated maximum left thumb abduction was undertaken by twenty-two participants twice, once in the morning (8 AM) and once in the evening (8 PM) on separate occasions. Saliva was assayed for cortisol concentration. Motor performance, quantified by measuring maximum left thumb abduction acceleration, significantly increased by 28% following training. Neuroplastic changes in corticomotor excitability of abductor pollicis brevis, quantified with TMS, increased significantly by 23% following training. Training-related motor performance improvements and neuroplasticity were unaffected by time of day and salivary cortisol concentration. Although similar neural elements and processes contribute to motor learning, training-induced neuroplasticity, and TMS-induced neuroplasticity, our findings suggest that the influence of time of day and cortisol differs for these three interventions. Martin V. Sale, Michael C. Ridding, and Michael A. Nordstrom Copyright © 2013 Martin V. Sale et al. All rights reserved. Wed, 13 Mar 2013 11:05:38 +0000 http://www.hindawi.com/journals/np/2013/639430/ The splenium of the corpus callosum connects the posterior cortices with fibers varying in size from thin late-myelinating axons in the anterior part, predominantly connecting parietal and temporal areas, to thick early-myelinating fibers in the posterior part, linking primary and secondary visual areas. In the adult human brain, the function of the splenium in a given area is defined by the specialization of the area and implemented via excitation and/or suppression of the contralateral homotopic and heterotopic areas at the same or different level of visual hierarchy. These mechanisms are facilitated by interhemispheric synchronization of oscillatory activity, also supported by the splenium. In postnatal ontogenesis, structural MRI reveals a protracted formation of the splenium during the first two decades of human life. In doing so, the slow myelination of the splenium correlates with the formation of interhemispheric excitatory influences in the extrastriate areas and the EEG synchronization, while the gradual increase of inhibitory effects in the striate cortex is linked to the local inhibitory circuitry. Reshaping interactions between interhemispherically distributed networks under various perceptual contexts allows sparsification of responses to superfluous information from the visual environment, leading to a reduction of metabolic and structural redundancy in a child's brain. Maria G. Knyazeva Copyright © 2013 Maria G. Knyazeva. All rights reserved. Sun, 24 Feb 2013 11:07:05 +0000 http://www.hindawi.com/journals/np/2013/149060/ Numerous studies have investigated the formation of interhemispheric connections which are involved in high-ordered functions of the cerebral cortex in eutherian animals, including humans. The development of callosal axons, which transfer and integrate information between the right/left hemispheres and represent the most prominent commissural system, must be strictly regulated. From the beginning of their growth, until reaching their targets in the contralateral cortex, the callosal axons are guided mainly by two environmental cues: (1) the midline structures and (2) neighboring? axons. Recent studies have shown the importance of axona guidance by such cues and the underlying molecular mechanisms. In this paper, we review these guidance mechanisms during the development of the callosal neurons. Midline populations express and secrete guidance molecules, and “pioneer” axons as well as interactions between the medial and lateral axons are also involved in the axon pathfinding of the callosal neurons. Finally, we describe callosal dysgenesis in humans and mice, that results from a disruption of these navigational mechanisms. Mitsuaki Nishikimi, Koji Oishi, and Kazunori Nakajima Copyright © 2013 Mitsuaki Nishikimi et al. All rights reserved. Thu, 21 Feb 2013 13:39:39 +0000 http://www.hindawi.com/journals/np/2013/258582/ Age-related brain injuries including stroke are a leading cause of morbidity and mental disability worldwide. Most patients who survive stroke experience some degree of recovery. The restoration of lost functions can be explained by neuronal plasticity, understood as brain ability to reorganize and remodel itself in response to changed environmental requirements. However, stroke triggers a cascade of events which may prevent the normal development of the plastic changes. One of them may be inflammatory response initiated immediately after stroke, which has been found to contribute to neuronal injury. Some recent evidence though has suggested that inflammatory reaction can be also neuroprotective. This paper attempts to discuss the influence of poststroke inflammatory response on brain plasticity and stroke outcome. We also describe the recent anti-inflammatory strategies that have been effective for recovery in experimental stroke. Monika Liguz-Lecznar and Malgorzata Kossut Copyright © 2013 Monika Liguz-Lecznar and Malgorzata Kossut. All rights reserved. Thu, 14 Feb 2013 18:59:20 +0000 http://www.hindawi.com/journals/np/2013/251308/ The concept of a topographical map of the corpus callosum (CC) has emerged from human lesion studies and from electrophysiological and anatomical tracing investigations in other mammals. Over the last few years a rising number of researchers have been reporting functional magnetic resonance imaging (fMRI) activation in white matter, particularly the CC. In this study the scope for describing CC topography with fMRI was explored by evoking activation through simple sensory stimulation and motor tasks. We reviewed our published and unpublished fMRI and diffusion tensor imaging data on the cortical representation of tactile, gustatory, auditory, and visual sensitivity and of motor activation, obtained in 36 normal volunteers and in 6 patients with partial callosotomy. Activation foci were consistently detected in discrete CC regions: anterior (taste stimuli), central (motor tasks), central and posterior (tactile stimuli), and splenium (auditory and visual stimuli). Reconstruction of callosal fibers connecting activated primary gustatory, motor, somatosensory, auditory, and visual cortices by diffusion tensor tracking showed bundles crossing, respectively, through the genu, anterior and posterior body, and splenium, at sites harboring fMRI foci. These data confirm that the CC commissure has a topographical organization and demonstrate that its functional topography can be explored with fMRI. Mara Fabri and Gabriele Polonara Copyright © 2013 Mara Fabri and Gabriele Polonara. All rights reserved. Thu, 14 Feb 2013 16:07:23 +0000 http://www.hindawi.com/journals/np/2013/196848/ The ubiquitin-proteasome system (UPS) is most widely known for its role in intracellular protein degradation; however, in the decades since its discovery, ubiquitination has been associated with the regulation of a wide variety of cellular processes. The addition of ubiquitin tags, either as single moieties or as polyubiquitin chains, has been shown not only to mediate degradation by the proteasome and the lysosome, but also to modulate protein function, localization, and endocytosis. The UPS plays a particularly important role in neurons, where local synthesis and degradation work to balance synaptic protein levels at synapses distant from the cell body. In recent years, the UPS has come under increasing scrutiny in neurons, as elements of the UPS have been found to regulate such diverse neuronal functions as synaptic strength, homeostatic plasticity, axon guidance, and neurite outgrowth. Here we focus on recent advances detailing the roles of the UPS in regulating the morphogenesis of axons, dendrites, and dendritic spines, with an emphasis on E3 ubiquitin ligases and their identified regulatory targets. Andrew M. Hamilton and Karen Zito Copyright © 2013 Andrew M. Hamilton and Karen Zito. All rights reserved. Tue, 12 Feb 2013 13:57:51 +0000 http://www.hindawi.com/journals/np/2013/394946/ In a recent article I reviewed an influential theory of sleep function, the “synaptic homeostasis hypothesis (SHY.)” According to SHY, sleep renormalizes synapses that are potentiated during prior wakefulness. I concluded that while SHY is a seminal theory with important implications about sleep function and the brain, its underlying mechanisms are poorly defined. In an accompanying article, the authors of SHY responded at length. Their reply is thoughtful and provocative, but unfortunately many of the points I raised were not accurately represented or addressed. In this brief commentary, I attempt to clarify some points of confusion. I also explain why any theory of sleep function is incomplete without an understanding of the underlying cellular mechanisms. Marcos Gabriel Frank Copyright © 2013 Marcos Gabriel Frank. All rights reserved. Sun, 03 Feb 2013 08:08:46 +0000 http://www.hindawi.com/journals/np/2013/432057/ The human brain is made up of an extensive network of neurons that communicate by forming specialized connections called synapses. The amount, location, and dynamic turnover of synaptic proteins, including neurotransmitter receptors and synaptic scaffolding molecules, are under complex regulation and play a crucial role in synaptic connectivity and plasticity, as well as in higher brain functions. An increasing number of studies have established ubiquitination and proteasome-mediated degradation as universal mechanisms in the control of synaptic protein homeostasis. In this paper, we focus on the role of the ubiquitin-proteasome system (UPS) in the turnover of major neurotransmitter receptors, including glutamatergic and nonglutamatergic receptors, as well as postsynaptic receptor-interacting proteins. Amy W. Lin and Heng-Ye Man Copyright © 2013 Amy W. Lin and Heng-Ye Man. All rights reserved. Mon, 28 Jan 2013 13:29:09 +0000 http://www.hindawi.com/journals/np/2013/359532/ Background. The etiology of motor impairments in preterm infants is multifactorial and incompletely understood. Whether corpus callosum development is related to impaired motor function is unclear. Potential associations between motor-related measures and diffusion tensor imaging (DTI) of the corpus callosum in preterm infants were explored. Methods. Eight very preterm infants (gestational age of 28–32 weeks) underwent the Hammersmith neonatal neurological examination and DTI assessments at gestational age of 42 weeks. The total Hammersmith score and a motor-specific score (sum of Hammersmith motor subcategories) were calculated. Six corpus callosum regions of interest were defined on the mid-sagittal DTI slice—genu, rostral body, anterior midbody, posterior midbody, isthmus, and splenium. The fractional anisotropy (FA) and mean diffusivity (MD) of these regions were computed, and correlations between these and Hammersmith measures were sought. Results. Anterior midbody FA measures correlated positively with total Hammersmith (rho , ) and motor-specific scores (rho , ). Total Hammersmith scores also negatively correlated with anterior midbody MD measures (rho , ). Discussion. These results suggest the integrity of corpus callosum axons, particularly anterior midbody axons, is important in mediating neurological functions. Greater callosal maturation was associated with greater motor function. Corpus callosum DTI may prove to be a valuable screening or prognostic marker. Preethi Mathew, Kerstin Pannek, Pamela Snow, M. Giulia D'Acunto, Andrea Guzzetta, Stephen E. Rose, Paul B. Colditz, and Simon Finnigan Copyright © 2013 Preethi Mathew et al. All rights reserved. Thu, 17 Jan 2013 17:41:23 +0000 http://www.hindawi.com/journals/np/2013/709732/ Physical exercise effects on brain health and cognitive performance have been described. Synaptic remodeling in hippocampus induced by physical exercise has been described in animal models, but the underlying mechanisms remain poorly understood. Changes in astrocytes, the glial cells involved in synaptic remodeling, need more characterization. We investigated the effect of moderate treadmill exercise (20 min/day) for 4 weeks on some parameters of astrocytic activity in rat hippocampal slices, namely, glial fibrillary acidic protein (GFAP), glutamate uptake and glutamine synthetase (GS) activities, glutathione content, and S100B protein content and secretion, as well as brain-derived neurotrophic factor (BDNF) levels and glucose uptake activity in this tissue. Results show that moderate treadmill exercise was able to induce a decrease in GFAP content (evaluated by ELISA and immunohistochemistry) and an increase in GS activity. These changes could be mediated by corticosterone, whose levels were elevated in serum. BDNF, another putative mediator, was not altered in hippocampal tissue. Moreover, treadmill exercise caused a decrease in NO content. Our data indicate specific changes in astrocyte markers induced by physical exercise, the importance of studying astrocytes for understanding brain plasticity, as well as reinforce the relevance of physical exercise as a neuroprotective strategy. Caren Bernardi, Ana Carolina Tramontina, Patrícia Nardin, Regina Biasibetti, Ana Paula Costa, Adriana Fernanda Vizueti, Cristiane Batassini, Lucas Silva Tortorelli, Krista Minéia Wartchow, Márcio Ferreira Dutra, Larissa Bobermin, Patrícia Sesterheim, André Quincozes-Santos, Jaqueline de Souza, and Carlos Alberto Gonçalves Copyright © 2013 Caren Bernardi et al. All rights reserved. Thu, 17 Jan 2013 16:55:21 +0000 http://www.hindawi.com/journals/np/2013/565167/ Long-term potentiation (LTP) which has long been considered a cellular model for learning and memory is defined as a lasting enhancement in synaptic transmission efficacy. This cellular mechanism has been demonstrated reliably in the hippocampus and the amygdala—two limbic structures implicated in learning and memory. Earlier studies reported on the ability of cortical stimulation of the entorhinal cortex to induce LTP simultaneously in the two sites. However, to retain a stable baseline of comparison with the majority of the LTP literature, it is important to investigate the ability of fiber stimulation such as perforant path activation to induce LTP concurrently in both structures. Therefore, in this paper we report on concurrent LTP in the basolateral amygdala (BLA) and the dentate gyrus (DG) subfield of the hippocampus induced by theta burst stimulation of perforant path fibers in freely behaving Sprague-Dawley rats. Our results indicate that while perforant path-evoked potentials in both sites exhibit similar triphasic waveforms, the latency and amplitude of BLA responses were significantly shorter and smaller than those of DG. In addition, we observed no significant differences in either the peak level or the duration of LTP between DG and BLA. J. Harry Blaise and Rachel A. Hartman Copyright © 2013 J. Harry Blaise and Rachel A. Hartman. All rights reserved. Mon, 31 Dec 2012 16:36:41 +0000 http://www.hindawi.com/journals/np/2012/854285/ Adult neurogenesis, the process of generating new neurons from neural stem cells, plays significant roles in synaptic plasticity, memory, and mood regulation. In the mammalian brain, it continues to occur well into adulthood in discrete regions, namely, the hippocampus and olfactory bulb. During the past decade, significant progress has been made in understanding the mechanisms regulating adult hippocampal neurogenesis and its role in the etiology of mental disorders. In addition, adult hippocampal neurogenesis is highly correlated with the remission of the antidepressant effect. In this paper, we discuss three major psychiatric disorders, depression, schizophrenia, and drug addiction, in light of preclinical evidence used in establishing the neurobiological significance of adult neurogenesis. We interpret the significance of these results and pose questions that remain unanswered. Potential treatments which include electroconvulsive therapy, deep brain stimulation, chemical antidepressants, and exercise therapy are discussed. While consensus lacks on specific mechanisms, we highlight evidence which indicates that these treatments may function via an increase in neural progenitor proliferation and changes to the hippocampal circuitry. Establishing a significant role of adult neurogenesis in the pathogenicity of psychiatric disorders may hold the key to potential strategies toward effective treatment. Heechul Jun, Syed Mohammed Qasim Hussaini, Michael J. Rigby, and Mi-Hyeon Jang Copyright © 2012 Heechul Jun et al. All rights reserved. Wed, 26 Dec 2012 10:21:05 +0000 http://www.hindawi.com/journals/np/2012/823285/ The corpus callosum, which is the largest white matter structure in the human brain, connects the 2 cerebral hemispheres. It plays a crucial role in maintaining the independent processing of the hemispheres and in integrating information between both hemispheres. The functional integrity of interhemispheric interactions can be tested electrophysiologically in humans by using transcranial magnetic stimulation, electroencephalography, and functional magnetic resonance imaging. As a brain structural imaging, diffusion tensor imaging has revealed the microstructural connectivity underlying interhemispheric interactions. Sex, age, and motor training in addition to the size of the corpus callosum influence interhemispheric interactions. Several neurological disorders change hemispheric asymmetry directly by impairing the corpus callosum. Moreover, stroke lesions and unilateral peripheral impairments such as amputation alter interhemispheric interactions indirectly. Noninvasive brain stimulation changes the interhemispheric interactions between both motor cortices. Recently, these brain stimulation techniques were applied in the clinical rehabilitation of patients with stroke by ameliorating the deteriorated modulation of interhemispheric interactions. Here, we review the interhemispheric interactions and mechanisms underlying the pathogenesis of these interactions and propose rehabilitative approaches for appropriate cortical reorganization. Naoyuki Takeuchi, Yutaka Oouchida, and Shin-Ichi Izumi Copyright © 2012 Naoyuki Takeuchi et al. All rights reserved. Mon, 24 Dec 2012 11:07:00 +0000 http://www.hindawi.com/journals/np/2012/768259/ Marie-Hélène Canu, Jacques-Olivier Coq, Mary F. Barbe, and Hubert R. Dinse Copyright © 2012 Marie-Hélène Canu et al. All rights reserved. Sun, 23 Dec 2012 08:27:10 +0000 http://www.hindawi.com/journals/np/2012/168297/ J. Tillein, S. Heid, E. Lang, R. Hartmann, and A. Kral Copyright © 2012 J. Tillein et al. All rights reserved. Thu, 20 Dec 2012 18:13:52 +0000 http://www.hindawi.com/journals/np/2012/352829/ SCRAPPER, which is an F-box protein encoded by FBXL20, regulates the frequency of the miniature excitatory synaptic current through the ubiquitination of Rab3-interacting molecule 1. Here, we recorded the induction of long-term potentiation/depression (LTP/LTD) in CA3-CA1 synapses in E3 ubiquitin ligase SCRAPPER-deficient hippocampal slices. Compared to wild-type mice, Scrapper-knockout mice exhibited LTDs with smaller magnitudes after induction with low-frequency stimulation and LTPs with larger magnitudes after induction with tetanus stimulation. These findings suggest that SCRAPPER regulates the threshold of bidirectional synaptic plasticity and, therefore, metaplasticity. Hiroshi Takagi, Mitsutoshi Setou, Seiji Ito, and Ikuko Yao Copyright © 2012 Hiroshi Takagi et al. All rights reserved. Tue, 18 Dec 2012 14:43:02 +0000 http://www.hindawi.com/journals/np/2012/892749/ Posttranslational modification of proteins by ubiquitin has emerged as a critical regulator of synapse development and function. Ubiquitination is a reversible modification mediated by the concerted action of a large number of specific ubiquitin ligases and ubiquitin proteases, called deubiquitinating enzymes (DUBs). The balance of activity of these enzymes determines the localization, function, and stability of target proteins. While some DUBs counter the action of specific ubiquitin ligases by removing ubiquitin and editing ubiquitin chains, other DUBs function more generally to maintain the cellular pool of free ubiquitin monomers. The importance of DUB function at the synapse is underscored by the association of specific mutations in DUB genes with several neurological disorders. Over the last decade, although much research has led to the identification and characterization of many ubiquitin ligases at the synapse, our knowledge of the relevant DUBs that act at the synapse has lagged. This review is focused on highlighting our current understanding of DUBs that regulate synaptic function and the diseases that result from dysfunction of these DUBs. Jennifer R. Kowalski and Peter Juo Copyright © 2012 Jennifer R. Kowalski and Peter Juo. All rights reserved. Thu, 06 Dec 2012 12:14:21 +0000 http://www.hindawi.com/journals/np/2012/627816/ To perform strictly unilateral movements, the brain relies on a large cortical and subcortical network. This network enables healthy adults to perform complex unimanual motor tasks without the activation of contralateral muscles. However, mirror movements (involuntary movements in ipsilateral muscles that can accompany intended movement) can be seen in healthy individuals if a task is complex or fatiguing, in childhood, and with increasing age. Lateralization of movement depends on complex interhemispheric communication between cortical (i.e., dorsal premotor cortex, supplementary motor area) and subcortical (i.e., basal ganglia) areas, probably coursing through the corpus callosum (CC). Here, we will focus on transcallosal interhemispheric inhibition (IHI), which facilitates complex unilateral movements and appears to play an important role in handedness, pathological conditions such as Parkinson’s disease, and stroke recovery. Vincent Beaulé, Sara Tremblay, and Hugo Théoret Copyright © 2012 Vincent Beaulé et al. All rights reserved. Mon, 26 Nov 2012 16:27:12 +0000 http://www.hindawi.com/journals/np/2012/902510/ ZENK expression in vocal nuclei is associated with singing behavior. Area X is an important nucleus for learning and stabilizing birdsong. ZENK expression is higher in Area X compared to that in other vocal nuclei when birds are singing. To reveal the relationship between the ZENK expression in Area X and song crystallization, immunohistochemistry was used to detect ZENK protein expression in Area X after the unilateral vocal nerve (tracheosyringeal nerve) section in adult male zebra finches. Sham operations had no effect on song. In contrast, section of unilateral vocal nerve could induce song decrystallization at the 7th day after the surgery. The spectral and the temporal features of birdsong were distorted more significantly in the right-side vocal nerve section than in the left-side vocal nerve section. In addition, after surgery, ZENK expression was higher in the right-side of Area X than in the left-side. These results indicate that the vocal nerve innervations probably are right-side dominant. ZENK expression in both sides of Area X decreased, as compared to control group after surgery, which suggests that the ZENK expression in Area X is related to birdsong crystallization, and that there is cooperation between the Area X in AFP and syrinx nerve. Congshu Liao and Dongfeng Li Copyright © 2012 Congshu Liao and Dongfeng Li. All rights reserved. Mon, 19 Nov 2012 13:20:57 +0000 http://www.hindawi.com/journals/np/2012/797295/ Callosal axon projections are among the major long-range axonal projections in the mammalian brain. They are formed during the prenatal and early postnatal periods in the mouse, and their development relies on both activity-independent and -dependent mechanisms. In this paper, we review recent findings about the roles of neuronal activity in callosal axon projections. In addition to the well-documented role of sensory-driven neuronal activity, recent studies using in utero electroporation demonstrated an essential role of spontaneous neuronal activity generated in neonatal cortical circuits. Both presynaptic and postsynaptic neuronal activities are critically involved in the axon development. Studies have begun to reveal intracellular signaling pathway which works downstream of neuronal activity. We also review several distinct patterns of neuronal activity observed in the developing cerebral cortex, which might play roles in activity-dependent circuit construction. Such neuronal activity during the neonatal period can be disrupted by genetic factors, such as mutations in ion channels. It has been speculated that abnormal activity caused by such factors may affect activity-dependent circuit construction, leading to some developmental disorders. We discuss a possibility that genetic mutation in ion channels may impair callosal axon projections through an activity-dependent mechanism. Yoshiaki Tagawa and Tomoo Hirano Copyright © 2012 Yoshiaki Tagawa and Tomoo Hirano. All rights reserved.