Xiaotong Zhang, Zhaocong Chen, Na Li, Jingfeng Liang, Y. Zou, Huixiang Wu, Z. Kang, Z. Dou, Weihong Qiu
{"title":"Regional Alteration within the Cerebellum and the Reorganization of the Cerebrocerebellar System following Poststroke Aphasia","authors":"Xiaotong Zhang, Zhaocong Chen, Na Li, Jingfeng Liang, Y. Zou, Huixiang Wu, Z. Kang, Z. Dou, Weihong Qiu","doi":"10.1155/2022/3481423","DOIUrl":"https://doi.org/10.1155/2022/3481423","url":null,"abstract":"Recently, an increasing number of studies have highlighted the role of the cerebellum in language processing. However, the role of neural reorganization within the cerebellum as well as within the cerebrocerebellar system caused by poststroke aphasia remains unknown. To solve this problem, in the present study, we investigated regional alterations of the cerebellum as well as the functional reorganization of the cerebrocerebellar circuit by combining structural and resting-state functional magnetic resonance imaging (fMRI) techniques. Twenty patients diagnosed with aphasia following left-hemispheric stroke and 20 age-matched healthy controls (HCs) were recruited in this study. The Western Aphasia Battery (WAB) test was used to assess the participants' language ability. Gray matter volume, spontaneous brain activity, functional connectivity, and effective connectivity were examined in each participant. We discovered that gray matter volumes in right cerebellar lobule VI and right Crus I were significantly lower in the patient group, and the brain activity within these regions was significantly correlated with WAB scores. We also discovered decreased functional connectivity within the crossed cerebrocerebellar circuit, which was significantly correlated with WAB scores. Moreover, altered information flow between the cerebellum and the contralateral cerebrum was found. Together, our findings provide evidence for regional alterations within the cerebellum and the reorganization of the cerebrocerebellar system following poststroke aphasia and highlight the important role of the cerebellum in language processing within aphasic individuals after stroke.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"1 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80437744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Plasticity of the Central Nervous System Involving Peripheral Nerve Transfer","authors":"Jun Shen","doi":"10.1155/2022/5345269","DOIUrl":"https://doi.org/10.1155/2022/5345269","url":null,"abstract":"Peripheral nerve injury can lead to partial or complete loss of limb function, and nerve transfer is an effective surgical salvage for patients with these injuries. The inability of deprived cortical regions representing damaged nerves to overcome corresponding maladaptive plasticity after the reinnervation of muscle fibers and sensory receptors is thought to be correlated with lasting and unfavorable functional recovery. However, the concept of central nervous system plasticity is rarely elucidated in classical textbooks involving peripheral nerve injury, let alone peripheral nerve transfer. This article is aimed at providing a comprehensive understanding of central nervous system plasticity involving peripheral nerve injury by reviewing studies mainly in human or nonhuman primate and by highlighting the functional and structural modifications in the central nervous system after peripheral nerve transfer. Hopefully, it will help surgeons perform successful nerve transfer under the guidance of modern concepts in neuroplasticity.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"64 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89330226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hao Yu, Fei Xu, Xiangmei Hu, Yanni Tu, Qiuyu Zhang, Zheng Ye, T. Hua
{"title":"Mechanisms of Surround Suppression Effect on the Contrast Sensitivity of V1 Neurons in Cats","authors":"Hao Yu, Fei Xu, Xiangmei Hu, Yanni Tu, Qiuyu Zhang, Zheng Ye, T. Hua","doi":"10.1155/2022/5677655","DOIUrl":"https://doi.org/10.1155/2022/5677655","url":null,"abstract":"Surround suppression (SS) is a phenomenon that a neuron's response to visual stimuli within the classical receptive field (cRF) is suppressed by a concurrent stimulation in the surrounding receptive field (sRF) beyond the cRF. Studies show that SS affects neuronal response contrast sensitivity in the primary visual cortex (V1). However, the underlying mechanisms remain unclear. Here, we examined SS effect on the contrast sensitivity of cats' V1 neurons with different preferred SFs using external noise-masked visual stimuli and perceptual template model (PTM) analysis at the system level. The contrast sensitivity was evaluated by the inverted threshold contrast of neurons in response to circular gratings of different contrasts in the cRF with or without an annular grating in the sRF. Our results showed that SS significantly reduced the contrast sensitivity of cats' V1 neurons. The SS-induced reduction of contrast sensitivity was not correlated with SS strength but was dependent on neuron's preferred SF, with a larger reduction for neurons with low preferred SFs than those with high preferred SFs. PTM analysis of threshold versus external noise contrast (TvC) functions indicated that SS decreased contrast sensitivity by increasing both the internal additive noise and impact of external noise for neurons with low preferred SFs, but improving only internal additive noise for neurons with high preferred SFs. Furthermore, the SS effect on the contrast-response function of low- and high-SF neurons also exhibited different mechanisms in contrast gain and response gain. Collectively, these results suggest that the mechanisms of SS effect on neuronal contrast sensitivity may depend on neuronal populations with different SFs.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"123 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85669508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Effects of the Biceps Brachii and Brachioradialis on Elbow Flexor Muscle Strength and Spasticity in Stroke Patients","authors":"Binbin Yu, Xintong Zhang, Yihui Cheng, Lingling Liu, YanJiang, Jiayue Wang, Xiao Lu","doi":"10.1155/2022/1295908","DOIUrl":"https://doi.org/10.1155/2022/1295908","url":null,"abstract":"Objective Muscle weakness and spasticity are common consequences of stroke, leading to a decrease in physical activity. The effective implementation of precision rehabilitation requires detailed rehabilitation evaluation. We aimed to analyze the surface electromyography (sEMG) signal features of elbow flexor muscle (biceps brachii and brachioradialis) spasticity in maximum voluntary isometric contraction (MVIC) and fast passive extension (FPE) in stroke patients and to explore the main muscle groups that affect the active movement and spasticity of the elbow flexor muscles to provide an objective reference for optimizing stroke rehabilitation. Methods Fifteen patients with elbow flexor spasticity after stroke were enrolled in this study. sEMG signals of the paretic and nonparetic elbow flexor muscles (biceps and brachioradialis) were detected during MVIC and FPE, and root mean square (RMS) values were calculated. The RMS values (mean and peak) of the biceps and brachioradialis were compared between the paretic and nonparetic sides. Additionally, the correlation between the manual muscle test (MMT) score and the RMS values (mean and peak) of the paretic elbow flexors during MVIC was analyzed, and the correlation between the modified Ashworth scale (MAS) score and the RMS values (mean and peak) of the paretic elbow flexors during FPE was analyzed. Results During MVIC exercise, the RMS values (mean and peak) of the biceps and brachioradialis on the paretic side were significantly lower than those on the nonparetic side (p < 0.01), and the RMS values (mean and peak) of the bilateral biceps were significantly higher than those of the brachioradialis (p < 0.01). The MMT score was positively correlated with the mean and peak RMS values of the paretic biceps and brachioradialis (r = 0.89, r = 0.91, r = 0.82, r = 0.85; p < 0.001). During FPE exercise, the RMS values (mean and peak) of the biceps and brachioradialis on the paretic side were significantly higher than those on the nonparetic side (p < 0.01), and the RMS values (mean and peak) of the brachioradialis on the paretic side were significantly higher than those of the biceps (p < 0.01). TheMAS score was positively correlated with the mean RMS of the paretic biceps and brachioradialis (r = 0.62, p = 0.021; r = 0.74, p = 0.004), and the MAS score was positively correlated with the peak RMS of the paretic brachioradialis (r = 0.59, p = 0.029) but had no significant correlation with the peak RMS of the paretic biceps (r = 0.49, p > 0.05). Conclusions The results confirm that the biceps is a vital muscle in active elbow flexion and that the brachioradialis plays an important role in elbow flexor spasticity, suggesting that the biceps should be the focus of muscle strength training of the elbow flexors and that the role of the brachioradialis should not be ignored in the treatment of elbow flexor spasticity. This study also confirmed the application value of sEMG in the objective assessment of individual","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"1 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90183998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neural PlasticityPub Date : 2022-02-22DOI: 10.21203/rs.3.rs-1344273/v1
Karina Hernández Mercado, Araceli Martínez Moreno, Luis Francisco Rodríguez Durán, M. Escobar, A. Zepeda
{"title":"Progression in Time of Dentate Gyrus Granule Cell Layer Widening due to Excitotoxicity Occurs along In Vivo LTP Reinstatement and Contextual Fear Memory Recovery","authors":"Karina Hernández Mercado, Araceli Martínez Moreno, Luis Francisco Rodríguez Durán, M. Escobar, A. Zepeda","doi":"10.21203/rs.3.rs-1344273/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-1344273/v1","url":null,"abstract":"The dentate gyrus (DG) is the gateway of sensory information arriving from the perforant pathway (PP) to the hippocampus. The adequate integration of incoming information into the DG is paramount in the execution of hippocampal-dependent cognitive functions. An abnormal DG granule cell layer (GCL) widening due to granule cell dispersion has been reported under hyperexcitation conditions in animal models as well as in patients with mesial temporal lobe epilepsy, but also in patients with no apparent relation to epilepsy. Strikingly, it is unclear whether the presence and severity of GCL widening along time affect synaptic processing arising from the PP and alter the performance in hippocampal-mediated behaviors. To evaluate the above, we injected excitotoxic kainic acid (KA) unilaterally into the DG of mice and analyzed the evolution of GCL widening at 10 and 30 days post injection (dpi), while analyzing if KA-induced GCL widening affected in vivo long-term potentiation (LTP) in the PP-DG pathway, as well as the performance in learning and memory through contextual fear conditioning. Our results show that at 10 dpi, when a subtle GCL widening was observed, LTP induction, as well as contextual fear memory, were impaired. However, at 30 dpi when a pronounced increase in GCL widening was found, LTP induction and contextual fear memory were already reestablished. These results highlight the plastic potential of the DG to recover some of its functions despite a major structural alteration such as abnormal GCL widening.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"32 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85590231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marcella M. Authiat, Emmanuelle Gruz-Gibelli, Julien Colas, E. Bianchi, Marta Garcia-Arauzo, P. Marin, F. Herrmann, A. Savioz
{"title":"Preferential Involvement of BRCA1/BARD1, Not Tip60/Fe65, in DNA Double-Strand Break Repair in Presenilin-1 P117L Alzheimer Models","authors":"Marcella M. Authiat, Emmanuelle Gruz-Gibelli, Julien Colas, E. Bianchi, Marta Garcia-Arauzo, P. Marin, F. Herrmann, A. Savioz","doi":"10.1155/2022/3172861","DOIUrl":"https://doi.org/10.1155/2022/3172861","url":null,"abstract":"Recently, we showed that DNA double-strand breaks (DSBs) are increased by the Aβ42-amyloid peptide and decreased by all-trans retinoic acid (RA) in SH-SY5Y cells and C57BL/6J mice. The present work was aimed at investigating DSBs in cells and murine models of Alzheimer's disease carrying the preseniline-1 (PS1) P117L mutation. We observed that DSBs could hardly decrease following RA treatment in the mutated cells compared to the wild-type cells. The activation of the amyloidogenic pathway is proposed in the former case as Aβ42- and RA-dependent DSBs changes were reproduced by an α-secretase and a γ-secretase inhibitions, respectively. Unexpectedly, the PS1 P117L cells showed lower DSB levels than the controls. As the DSB repair proteins Tip60 and Fe65 were less expressed in the mutated cell nuclei, they do not appear to contribute to this difference. On the contrary, full-length BRCA1 and BARD1 proteins were significantly increased in the chromatin compartment of the mutated cells, suggesting that they decrease DSBs in the pathological situation. These Western blot data were corroborated by in situ proximity ligation assays: the numbers of BRCA1-BARD1, not of Fe65-Tip60 heterodimers, were increased only in the mutated cell nuclei. RA also enhanced the expression of BARD1 and of the 90 kDa BRCA1 isoform. The increased BRCA1 expression in the mutated cells can be related to the enhanced difficulty to inhibit this pathway by BRCA1 siRNA in these cells. Overall, our study suggests that at earlier stages of the disease, similarly to PS1 P117L cells, a compensatory mechanism exists that decreases DSB levels via an activation of the BRCA1/BARD1 pathway. This supports the importance of this pathway in neuroprotection against Alzheimer's disease.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"40 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85382143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mai Sakai, Zhiqian Yu, Ryo Hirayama, Masaomi Nakasato, Yoshie Kikuchi, Chiaki Ono, H. Komatsu, M. Nakanishi, Hatsumi Yoshii, D. Stellwagen, T. Furuyashiki, M. Komatsu, Hiroaki Tomita
{"title":"Deficient Autophagy in Microglia Aggravates Repeated Social Defeat Stress-Induced Social Avoidance","authors":"Mai Sakai, Zhiqian Yu, Ryo Hirayama, Masaomi Nakasato, Yoshie Kikuchi, Chiaki Ono, H. Komatsu, M. Nakanishi, Hatsumi Yoshii, D. Stellwagen, T. Furuyashiki, M. Komatsu, Hiroaki Tomita","doi":"10.1155/2022/7503553","DOIUrl":"https://doi.org/10.1155/2022/7503553","url":null,"abstract":"Major depressive disorder (MDD) is associated with repeated exposure to environmental stress. Autophagy is activated under various stress conditions that are associated with several diseases in the brain. This study was aimed at elucidating the autophagy signaling changes in the prefrontal cortex (PFC) under repeated social defeat (RSD) to investigate the involvement of microglial autophagy in RSD-induced behavioral changes. We found that RSD stress, an animal model of MDD, significantly induced initial autophagic signals followed by increased transcription of autophagy-related genes (Atg6, Atg7, and Atg12) in the PFC. Similarly, significantly increased transcripts of ATGs (Atg6, Atg7, Atg12, and Atg5) were confirmed in the postmortem PFC of patients with MDD. The protein levels of the prefrontal cortical LC3B were significantly increased, whereas p62 was significantly decreased in the resilient but not in susceptible mice and patients with MDD. This indicates that enhanced autophagic flux may alleviate stress-induced depression. Furthermore, we identified that FKBP5, an early-stage autophagy regulator, was significantly increased in the PFC of resilient mice at the transcript and protein levels. In addition, the resilient mice exhibited enhanced autophagic flux in the prefrontal cortical microglia, and the autophagic deficiency in microglia aggravated RSD-induced social avoidance, indicating that microglial autophagy involves stress-induced behavioral changes.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"87 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73053966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neural PlasticityPub Date : 2021-03-29eCollection Date: 2021-01-01DOI: 10.1155/2021/8834645
Wojciech Kozubski, Kevin Ong, Wioletta Waleszczyk, Matthew Zabel, Jolanta Dorszewska
{"title":"Molecular Factors Mediating Neural Cell Plasticity Changes in Dementia Brain Diseases.","authors":"Wojciech Kozubski, Kevin Ong, Wioletta Waleszczyk, Matthew Zabel, Jolanta Dorszewska","doi":"10.1155/2021/8834645","DOIUrl":"https://doi.org/10.1155/2021/8834645","url":null,"abstract":"<p><p>Neural plasticity-the ability to alter a neuronal response to environmental stimuli-is an important factor in learning and memory. Short-term synaptic plasticity and long-term synaptic plasticity, including long-term potentiation and long-term depression, are the most-characterized models of learning and memory at the molecular and cellular level. These processes are often disrupted by neurodegeneration-induced dementias. Alzheimer's disease (AD) accounts for 50% of cases of dementia. Vascular dementia (VaD), Parkinson's disease dementia (PDD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD) constitute much of the remaining cases. While vascular lesions are the principal cause of VaD, neurodegenerative processes have been established as etiological agents of many dementia diseases. Chief among such processes is the deposition of pathological protein aggregates <i>in vivo</i> including <i>β</i>-amyloid deposition in AD, the formation of neurofibrillary tangles in AD and FTD, and the accumulation of Lewy bodies composed of <i>α</i>-synuclein aggregates in DLB and PDD. The main symptoms of dementia are cognitive decline and memory and learning impairment. Nonetheless, accurate diagnoses of neurodegenerative diseases can be difficult due to overlapping clinical symptoms and the diverse locations of cortical lesions. Still, new neuroimaging and molecular biomarkers have improved clinicians' diagnostic capabilities in the context of dementia and may lead to the development of more effective treatments. Both genetic and environmental factors may lead to the aggregation of pathological proteins and altered levels of cytokines, such that can trigger the formation of proinflammatory immunological phenotypes. This cascade of pathological changes provides fertile ground for the development of neural plasticity disorders and dementias. Available pharmacotherapy and disease-modifying therapies currently in clinical trials may modulate synaptic plasticity to mitigate the effects neuropathological changes have on cognitive function, memory, and learning. In this article, we review the neural plasticity changes seen in common neurodegenerative diseases from pathophysiological and clinical points of view and highlight potential molecular targets of disease-modifying therapies.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"8834645"},"PeriodicalIF":3.1,"publicationDate":"2021-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8021472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25589955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neural PlasticityPub Date : 2021-03-27eCollection Date: 2021-01-01DOI: 10.1155/2021/6612456
Ming Zhang, Yuqi Zhang, Zhihui Li, Li Hu, Yazhuo Kong
{"title":"Sexism-Related Stigma Affects Pain Perception.","authors":"Ming Zhang, Yuqi Zhang, Zhihui Li, Li Hu, Yazhuo Kong","doi":"10.1155/2021/6612456","DOIUrl":"https://doi.org/10.1155/2021/6612456","url":null,"abstract":"<p><p>People with stigmatized characteristics tend to be devalued by others in a given society. The negative experiences related to stigma cause individuals to struggle as they would if they were in physical pain and bring various negative outcomes in the way that physical pain does. However, it is unclear whether stigma related to one's identity would affect their perception of physical pain. To address this issue, using sexism-related paradigms, we found that females had reduced pain threshold/tolerance in the Cold Pressor Test (Experiment 1) and an increased rating for nociceptive laser stimuli with fixed intensity (Experiment 2). Additionally, we observed that there was a larger laser-evoked N1, an early laser-evoked P2, and a larger magnitude of low-frequency component in laser-evoked potentials (LEPs) in the stigma condition than in the control condition (Experiment 3). Our study provides behavioral and electrophysiological evidence that sexism-related stigma affects the pain perception of females.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"6612456"},"PeriodicalIF":3.1,"publicationDate":"2021-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25589953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neural PlasticityPub Date : 2021-03-25eCollection Date: 2021-01-01DOI: 10.1155/2021/6668389
Lijie Hao, Zhuoqin Yang
{"title":"Dynamical Mechanisms for Gene Regulation Mediated by Two Noncoding RNAs in Long-Term Memory Formation.","authors":"Lijie Hao, Zhuoqin Yang","doi":"10.1155/2021/6668389","DOIUrl":"https://doi.org/10.1155/2021/6668389","url":null,"abstract":"<p><p>Noncoding RNAs such as miRNAs and piRNAs have long-lasting effects on the regulation of gene expression involved in long-term synaptic changes. To characterize gene regulation mediated by small noncoding RNAs associated with long-term memory in <i>Aplysia</i>, we consider two noncoding RNAs stimulated by 5-HT into a gene regulatory network motif model, including miR-124 that binds to and inhibits the mRNA of CREB1 and piR-F that facilitates serotonin-dependent DNA methylation to lead to repression of CREB2. Codimension-1 and -2 bifurcation analyses of 5-HT regulating both miR-124 and piR-F and a negative feedback strength for oscillation reveal rich dynamical properties of bistability and oscillations robust to variations in all other parameters. More importantly, we verify three stimulus protocols of 5-HT in experiments by our model and find that application of five pulses of 5-HT leads to a transient decrease of miR-124 but increase of piR-F concentrations, which matters sustained high level of CREB1 concentration associated with long-term memory. Furthermore, we perform bifurcation analyses for the concentrations of miR-124 and piR-F as two parameters to explore dynamical mechanisms underlying the epigenetic regulation in long-term memory formation. This study provides insights into revealing regulatory roles of epigenetic changes in gene expression involving noncoding RNAs associated with synaptic plasticity.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"6668389"},"PeriodicalIF":3.1,"publicationDate":"2021-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25572930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}