Special Issues

Special Issue Title: Exploration of mechanisms in cortical plasticity

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· Deadline for manuscript submissions: 1 August 2020



Special Issue Editor

Guest Editor


Prof. Dr. Tetsuya Asakawa

1. Research Base of Traditional Chinese Medicine Syndrome, Fujian University of Traditional Chinese Medicine 
2. Department of Neurosurgery, Hamamatsu University School of Medicine. Handayama, 1-20-1, Higashi-ku, Hamamatsu-city, Shizuoka, 431-3192, Japan

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Interests: Neurology, functional neurosurgery, behavioral science, molecular imaging, neurophysiology, TCM research (herb, acupuncture, etc)



 Adjunct Research Assistant Prof. Rodolfo Gatto

 Department of Bioengineering, University of Illinois at Chicago, 851 S Morgan St, SEO 218 Chicago, IL 60607, USA

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Interests: Neuroimaging techniques & algorithms, neurodegenerative diseases and traumatic brain injury



Special Issue Information

Dear Colleagues,


Cortical plasticity, also known as neural plasticity, neuroplasticity or brain plasticity, is defined as a neurobiological ability of the nervous system to change its biophysiological functions by forming new neural connections. Therefore, it is a constant and dynamic remodeling process that allows the incorporation of new information. Such structural changes in neuronal connectivity, by cortical and subcortical rewiring of neuronal circuits, are extremely important mechanisms to adapt and survive continuously changing environments. Despite the increasing scientific attention to the cortical plasticity, its mechanisms have not been fully understood due to their complicated and multifold nature. In the last decades, the understanding of basic molecular, functional and associate ultrastructural remodeling mechanisms has gained momentum in diverse neuroscientific fields. With the recent advance of new genetic tools and non-invasive neuroimaging systems in the context of in vivo and in vitro studies, the assessment of synaptic and neuronal network changes across different cortical regions is achievable. Moreover, some of those techniques are making it possible to monitor in real-time new neural connections induced by several neurorehabilitation interventions. Such potential adaptability in neuronal connectivity has also been observed in the situation of aging, injury, and neurodegeneration as a potential therapeutic approached to restore the loss in several cortical functions. Furthermore, since most of the neuronal damages induced by diverse neurological diseases are irreversible, and the next-generation therapies like stem cell transplantation and gene therapy are far from been widely used in clinical practice, treatments associated with cortical plasticity are expected to improve the disease’s prognosis. In this topic, we are welcoming authors from any related basic and clinical fields to contribute with original research articles in a growing effort to illustrate different cortical plasticity mechanisms using diverse scientific methods. Therefore, the main goal of this topic is to provide the reader with a wide overview of current knowledge in the neuroplasticity field and the state-of-the-art application of novel cellular, animal and clinical experimental procedures to explore and enhance such mechanisms of neuronal restoration. Investigations using a “bench to bedside” translation approaches are particularly encouraged. Original research reports, review articles, communications, and perspectives are welcome in all areas pertinent to the topic.


Prof. Dr. Tetsuya Asakawa and Prof. Dr. Rodolfo G. Gatto

Guest Editor

 

Manuscript Submission Information

Manuscripts should be submitted online at https://jour.ipublishment.com/imr/access/login by registering and logging into this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Integrative Neuroscience is an international peer-reviewed open access quarterly journal published by IMR Press.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is $1500. We normally offer a discount greater than 30% (APC: $1050) to all contributors invited by the Editor-in-Chief, Guest Editor (GE) and Editorial board member. Submitted papers should be well formatted and use good English.


Keywords

Cortical plasticity, neuronal regeneration, neuronal and axonal connectivity, adaptative neuronal networks, neuronal restoration and repair, neurorehabilitation, neuroimaging



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Published Papers (8 papers)
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The Chinese herb Fructus Broussonetiae aids learning and memory in chronic cerebral hypoperfusion by reducing proinflammatory microglia activation in rats
Ping Liu, Li-ye Wang, Yu-qing Wang, Rong-liang Wang, Fang-fang Li, Sijia Zhang, Zhen Tao, Hai-ping Zhao, Zi-ping Han, Zhi-gang Chen, Yu-min Luo
Journal of Integrative Neuroscience    2020, 19 (1): 21-29.   DOI: 10.31083/j.jin.2020.01.1213
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The neuroprotective role of Fructus Broussonetiae in a model of chronic cerebral hypoperfusion with cognitive decline was focused on neural plasticity and microglia/macrophage polarization. Chronic cerebral hypoperfusion was induced by bilateral common carotid artery ligation. Fructus Broussonetiae shortened escape latency and added the number of platform crossings of rats, up-regulated the expression of synaptophysin in the gray matter and increased myelin basic protein expression in the white matter. Further mechanistic experiments were conducted to examine microglia activation and M1/M2 polarization. It was shown that Fructus Broussonetiae reduced the activation of microglia revealed by decreased expression of ionized calcium-binding adapter molecule-1, inhibited M1 polarization of microglia and improved microglial M2 polarization shown by down-regulated the expression of inducible nitric oxide synthase and Fc fragment of IgG receptor IIIa and up-regulated the expression of arginase-1. In conclusion, the Chinese herb Fructus Broussonetiae can improve cognitive function following chronic cerebral hypoperfusion by down-regulating the activation of microglia, inhibiting microglial M1 polarization, and improving neural plasticity.

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Can repetitive transcranial magnetic stimulation enhance motor outcomes in cerebral infarct patients?
Jun Young Kim, Mathieu Boudier-Revéret, Min Cheol Chang
Journal of Integrative Neuroscience    2020, 19 (1): 119-123.   DOI: 10.31083/j.jin.2020.01.20
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The effectiveness of repetitive transcranial magnetic stimulation on the post-stroke motor recovery is not apparent. To perform an accurate evaluation, we adjusted for critical factors that determine motor outcomes, including lesion location and the state of the corticospinal tract. We only included patients with cerebral infarct in the corona radiata and with corticospinal tract interruption, apparent on diffusion tensor tractography. We retrospectively enrolled 34 patients whose diffusion tensor tractography corticospinal tract was interrupted by a cerebral infarct. The corticospinal tract state of each patient was evaluated using diffusion tensor tractography. Of the 34 patients whose corticospinal tract was interrupted on diffusion tensor tractography, 12 patients underwent repetitive transcranial magnetic stimulation treatment at the early stage after cerebral infarct (repetitive transcranial magnetic stimulation group). In comparison, 22 patients did not receive repetitive transcranial magnetic stimulation treatment (non-repetitive transcranial magnetic stimulation group). High-frequency repetitive transcranial magnetic stimulation (10 Hz) was performed on the primary motor cortex of the affected hemisphere. At the six month evaluation after the onset of the infarct, motor function was measured in each patient. In both groups, compared to their states during the initial evaluation, significant improvement was found in all measurements of motor function. However, six months after onset, no significant differences between the two groups were found in these measurement scores. When a patient's CST is interrupted, high-frequency repetitive transcranial magnetic stimulation treatment at the early stage after cerebral infarct might have no additional therapeutic effect on motor outcome. Qualified randomized controlled trials are needed to support our findings further.

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Development of a novel gripping test for the evaluation of the finger fine motor ability in MPTP-treated monkeys
Susumu Kobayashi, Tetsuya Asakawa, Takao Nozaki, Kenji Sugiyama, Tetsuro Sameshima, Kazuhiko Kurozumi
Journal of Integrative Neuroscience    2020, 19 (2): 209-215.   DOI: 10.31083/j.jin.2020.02.158
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Assessing the finger fine motor ability is extremely important. However, conventional behavioral tests in monkeys are complicated and costly. We attempted to develop a new task to assess the precise finger grip in Parkinson's disease monkeys based on the principles of objectification, multipurpose, and simplification. This study involved seven adult male cynomolgus monkeys. A gripping test based on the previous food reaching test was developed. Parallel experiments of food reaching test and gripping test affected by the treatments of levodopa and deep brain stimulation of the subthalamic nucleus were performed to verify the utility of the gripping test. We found that gross motor ability (measured by food reaching test) could be significantly improved by both the subthalamic nucleus and levodopa administration, which reproduced the results of our previous study. The finger fine motor ability (measured by the gripping test) could be significantly improved by levodopa administration, but not by the subthalamic nucleus. Our results verified the utility and reliability of the gripping test, which is a simple, convenient, and objective task for evaluating the finger fine motor skill in Parkinson's disease monkeys. Mechanisms of the efficacy of deep brain stimulation on fine motor ability require further investigation.
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N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine attenuates oxygen-glucose deprivation and reoxygenation-induced cerebral ischemia-reperfusion injury via regulation of microRNAs
Tiansong Yang, Dongyan Wang, Yuanyuan Qu, Yulin Wang, Yuenan Feng, Yan Yang, Qiang Luo, Xiaowei Sun, Guoqiang Yu, Jia He, Zhongren Sun, Yulan Zhu
Journal of Integrative Neuroscience    2020, 19 (2): 303-311.   DOI: 10.31083/j.jin.2020.02.1236
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Cerebral ischemia-reperfusion injury is a common complication that occurs during stroke treatment. Increasingly, microRNAs have been found to participate in the modulation of neuron function; however, the role of microRNAs in cerebral ischemia-reperfusion injury remains unclear. We developed a mechanism of cerebral ischemia-reperfusion injury using a cellular model of oxygen-glucose deprivation and reoxygenation-induced injury in human neuroblastoma SH-SY5Y cells. We found that treatment of oxygen-glucose deprivation and reoxygenation promoted the apoptosis of SH-SY5Y cells. Analysis of microRNAs sequencing revealed that the expression of microRNA-27a-5p was induced, and microRNA-29b-3p expression was inhibited in neuroblastoma cells exposed to oxygen-glucose deprivation and reoxygenation. Either inhibition of microRNA-27a-5p or overexpression of microRNA-29b-3p mitigated oxygen-glucose deprivation and reoxygenation-induced cellular apoptosis. Bach1 was authenticated as a target gene of microRNA-27a-5p. Also, microRNA-27a-5p mediated the expression of Bach 1 along with its downstream signaling. N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine protected against oxygen-glucose deprivation and reoxygenation-induced apoptosis while decreasing miR-27a-5p expression and increasing microRNA-29b-3p expression. These results suggested that microRNA-27a-5p and microRNA-29b-3p may contribute to oxygen-glucose deprivation and reoxygenation-induced cellular injury. At the same time, N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine protects SH-SY5Y cells against oxygen-glucose deprivation and reoxygenation-induced injury partly through the inhibition of microRNA-27-a-5p and promotion of the Bach1/HO-1 signaling pathway.
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The effects of erythropoietin on neurogenesis after ischemic stroke
Si-Jia Zhang, Yu-Min Luo, Rong-Liang Wang
Journal of Integrative Neuroscience    2020, 19 (3): 561-570.   DOI: 10.31083/j.jin.2020.03.4
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Erythropoietin has been researched for its neuroprotective effects in ischemic stroke for over 30 years. Although erythropoietin can cause side effects that need to be controlled, it has been suggested to be effective in enhancing the prognosis of patients who are out of the therapeutic time window and have not received recombinant tissue plasminogen activator therapy. Studies on the mechanism of the function of erythropoietin have shown that it has various protective effects in ischemic brain injury after stroke, including promoting neurogenesis. In this review, we discuss the effects of erythropoietin on neurogenesis after ischemic brain injury and provide references for effective treatments for ischemic stroke, which is one of the leading causes of death worldwide.

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Molecular and microstructural biomarkers of neuroplasticity in neurodegenerative disorders through preclinical and diffusion magnetic resonance imaging studies
Rodolfo Gabriel Gatto
Journal of Integrative Neuroscience    2020, 19 (3): 571-592.   DOI: 10.31083/j.jin.2020.03.165
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Advances in the understanding of genetic and molecular mechanisms and imaging technologies have opened a new window of research possibilities to address dynamic processes associated with neuroplasticity in physiologically intact models of neurodegenerative diseases. This review aims to: (i) establish the most relevant molecular mechanisms, as well as cellular and structural biomarkers in the study of neuroplasticity; (ii) introduce different neurodegenerative diseases in animal models that contribute to our knowledge of neuroplasticity; and (iii) illustrate the capabilities and limitations of current diffusion magnetic resonance imaging techniques to study cortical plasticity, as well as the use of alternative diffusion models.

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A meta-analysis of case studies and clinical characteristics of hypertrophic olivary degeneration secondary to brainstem infarction
Yi-Lin Wang, Yan Gao, Ping-Ping He, Jiang-Ning Yin, Ruo-Fei Dong, Xin Li, Yu Fu, Hong Zhang
Journal of Integrative Neuroscience    2020, 19 (3): 507-511.   DOI: 10.31083/j.jin.2020.03.1238
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Transsynaptic degeneration in the cerebellum and brainstem may give rise to a rare neurological condition with various clinical manifestations, namely hypertrophic olivary degeneration. The classical manifestations of hypertrophic olivary degeneration comprise myoclonus, palatal tremor, ataxia, and ocular symptoms. Any lesions interrupting the dentate-rubro-olivary pathway, referred to as the anatomic Guillain-Mollaret triangle, contribute to the broad aetiologies of hypertrophic olivary degeneration. The clinical diagnosis depends primarily on the associated symptoms and the characteristic magnetic resonance imaging findings. Concerning treatment and prognosis, there are no widely accepted guidelines. Here, we identified 11 cases of hypertrophic olivary degeneration secondary to brainstem infarction from 1964 to the present. Combined with two of our cases, the clinical and imaging findings of 13 patients with hypertrophic olivary degeneration secondary to brainstem infarction were studied. A meta-analysis of case studies gives the correlation coefficient between infraction location and time to develop hypertrophic olivary degeneration as 0.217 (P = 0.393, P > 0.05). At the significance level of P < 0.05, there was no significant correlation between infraction location and time to develop hypertrophic olivary degeneration. The χ2 between infraction location and magnetic resonance imaging findings of hypertrophic olivary degeneration was 8.750 (P = 0.364, P > 0.05). At the significance level of P < 0.05, there was no significant correlation between infraction location and magnetic resonance imaging findings of hypertrophic olivary degeneration. Conclusion based on the analysis of available data suggests that when newly developed or progressive worsening motor symptoms are presented in patients with previous brainstem infarction, a diagnosis of hypertrophic olivary degeneration should be investigated.

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New molecular insights, innovative technologies, and medical approaches in the “Exploration of mechanisms in cortical plasticity”
Rodolfo G. Gatto, Tetsuya Asakawa
Journal of Integrative Neuroscience    2020, 19 (4): 733-734.   DOI: 10.31083/j.jin.2020.04.348
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