Browsing by Subject "Neuroplasticity"

Now showing 1 - 4 of 4
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    Differences in regional homogeneity between patients with Crohn's disease with and without abdominal pain revealed by resting-state functional magnetic resonance imaging
    (Wolters Kluwer, 2016-05) Bao, Chun-Hui; Liu, Peng; Liu, Hui-Rong; Wu, Lu-Yi; Jin, Xiao-Ming; Wang, Si-Yao; Shi, Yin; Zhang, Jian-Ye; Zeng, Xiao-Qing; Ma, Li-Li; Qin, Wei; Zhao, Ji-Meng; Calhoun, Vince D.; Tian, Jie; Wu, Huan-Gan; Medicine, School of Medicine
    Abnormal pain processing in the central nervous system may be related to abdominal pain in patients with Crohn's disease (CD). The purpose of this study was to investigate changes in resting-state brain activity in patients with CD in remission and its relationship with the presence of abdominal pain. Twenty-five patients with CD and with abdominal pain, 25 patients with CD and without abdominal pain, and 32 healthy subjects were scanned using a 3.0-T functional magnetic resonance imaging scanner. Regional homogeneity (ReHo) was used to assess resting-state brain activity. Daily pain scores were collected 1 week before functional magnetic resonance imaging. We found that patients with abdominal pain exhibited lower ReHo values in the insula, middle cingulate cortex (MCC), and supplementary motor area and higher ReHo values in the temporal pole. In contrast, patients without abdominal pain exhibited lower ReHo values in the hippocampal/parahippocampal cortex and higher ReHo values in the dorsomedial prefrontal cortex (all P < 0.05, corrected). The ReHo values of the insula and MCC were significantly negatively correlated with daily pain scores for patients with abdominal pain (r = -0.53, P = 0.008 and r = -0.61, P = 0.002, respectively). These findings suggest that resting-state brain activities are different between remissive patients with CD with and without abdominal pain and that abnormal activities in insula and MCC are closely related to the severity of abdominal pain.
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    Exploring propriospinal neuron-mediated neural circuit plasticity using recombinant viruses after spinal cord injury
    (Elsevier, 2022-03) Deng, Lingxiao; Ravenscraft, Baylen; Xu, Xiao-Ming; Neurological Surgery, School of Medicine
    Propriospinal neurons (PSNs) play a crucial role in motor control and sensory processing and contribute to plastic reorganization of spinal circuits responsible for recovery from spinal cord injury (SCI). Due to their scattered distribution and various intersegmental projection patterns, it is challenging to dissect the function of PSNs within the neuronal network. New genetically encoded tools, particularly cell-type–specific transgene expression methods using recombinant viral vectors combined with other genetic, pharmacologic, and optogenetic approaches, have enormous potential for visualizing PSNs in the neuronal circuits and monitoring and manipulating their activity. Furthermore, recombinant viral tools have been utilized to promote the intrinsic regenerative capacities of PSNs, towards manipulating the ‘hostile’ microenvironment for improving functional regeneration of PSNs. Here we summarize the latest development in this fast-moving field and provide a perspective for using this technology to dissect PSN physiological role in contributing to recovery of function after SCI.
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    Kinematic changes following robotic-assisted upper extremity rehabilitation in children with hemiplegia : dosage effects on movement time
    (2018-04-30) Cardinal, Ryan Edward; Altenburger, Peter; Fuchs, Robyn; Massie, Crystal; Warden, Stuart
    Background: Rehabilitation Robotics (RR) has become a more widely used and better understood treatment intervention and research tool in the last 15 years. Traditional research involves pre and post-test outcomes, making it difficult to analyze changes in behavior during the treatment process. Harnessing kinematics captured throughout each treatment allows motor learning to be quantified and questions of application and dosing to be answered. Objective: The aims of this secondary analysis were: (i) to investigate the impact of treatment presentation during RR on upper extremity movement time (mt) in children with hemiplegic cerebral palsy (CP) and (ii) to investigate the impact of training structure (dose and intensity) on mt in children with CP participating in RR. Methods: Subjects completed 16 intervention sessions of RR (2 x week; 8 weeks) with a total of 1,024 repetitions of movement per session and three assessments: pre, post and 6 month f/u. During each assessment and intervention, subjects completed “one-way record” assessments tracking performance on a planar task without robotic assistance. Kinematics from these records were extracted to assess subject performance over the course of and within sessions. Results: For all participants, a significant decrease in mt was found at post-test and follow-up. No significant differences were found in mt for age, severity or group placement. A significant interaction was found between treatment day, block and group (p = .033). Significant mt differences were found between the three blocks of intervention within individual days (p = .001). Specifically, significant differences were found over the last block of treatment (p = .032) and between successive treatment days (p = .001). Conclusion: The results indicate that for children with CP participating in RR, the number of repetitions per session is important. We hypothesized that children’s performance would plateau during a treatment day as attention waned, the opposite proved to be true. Despite the high-number of repetitions and associated cognitive demand, subjects’ performance actually trended upwards throughout the 1,024 repetitions suggesting that children were able to tolerate and learn from a high volume of repetitions.
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    Multi-animal model study reveals mutations in neural plasticity and nociception genes are linked to excessive alcohol drinking
    (Wiley, 2023) Muir, William M.; Lo, Chiao-Ling; Bell, Richard L.; Zhou, Feng C.; Medicine, School of Medicine
    Background: The basis for familial alcohol use disorder (AUD) remains an enigma due to various biological and societal confounds. The present study used three of the most adopted and documented rat models, combining the alcohol-preferring/non-alcohol-preferring (P/NP) lines and high alcohol-drinking/low alcohol-drinking (HAD/LAD) replicated lines, of AUD as examined through the lens of whole genomic analyses. Methods: We used complete genome sequencing of the P/NP lines and previously published sequences of the HAD/LAD replicates to enhance the discovery of variants associated with AUD and to remove confounding with genetic background and random genetic drift. Specifically, we used high-order statistical methods to search for genetic variants whose frequency changes in whole sets of gene ontologies corresponded with phenotypic changes in the direction of selection, that is, ethanol-drinking preference. Results: Our first finding was that in addition to variants causing translational changes, the principal genetic changes associated with drinking predisposition were silent mutations and mutations in the 3' untranslated regions (3'UTR) of genes. Neither of these types of mutations alters the amino acid sequence of the translated protein but they influence both the rate and conformation of gene transcription, including its stability and posttranslational events that alter gene efficacy. This finding argues for refocusing human genomic studies on changes in gene efficacy. Among the key ontologies identified were the central genes associated with the Na+ voltage-gated channels of neurons and glia (including the Scn1a, Scn2a, Scn2b, Scn3a, Scn7a, and Scn9a subtypes) and excitatory glutamatergic secretion (including Grm2 and Myo6), both of which are essential in neuroplasticity. In addition, we identified "Nociception or Sensory Perception of Pain," which contained variants in nociception (Arrb1, Ccl3, Ephb1) and enlist sodium (Scn1a, Scn2a, Scn2b, Scn3a, Scn7a), pain activation (Scn9a), and potassium channel (Kcna1) genes. Conclusion: The multi-model analyses used herein reduced the confounding effects of random drift and the "founders" genetic background. The most differentiated bidirectionally selected genes across all three animal models were Scn9a, Scn1a, and Kcna, all of which are annotated in the nociception ontology. The complexity of neuroplasticity and nociception adds strength to the hypothesis that neuroplasticity and pain (physical or psychological) are prominent phenotypes genetically linked to the development of AUD.