Brain plasticity is the basis for systems-level functional reorganization that promotes recovery in multiple sclerosis (MS). As inflammation interferes with plasticity, its pharmacological modulation may restore plasticity by promoting desired patterns of functional reorganization. Here, we tested the hypothesis that brain plasticity probed by a visuomotor adaptation task is impaired with MS inflammation and that pharmacological reduction of inflammation facilitates its restoration. MS patients were assessed twice before (sessions 1 and 2) and once after (session 3) the beginning of Interferon beta (IFN beta), using behavioural and structural MRI measures. During each session, 2 functional MRI runs of a visuomotor task, separated by 25-minutes of task practice, were performed. Within-session between-run change in task-related functional signal was our imaging marker of plasticity. During session 1, patients were compared with healthy controls. Comparison of patients' sessions 2 and 3 tested the effect of reduced inflammation on our imaging marker of plasticity. The proportion of patients with gadolinium-enhancing lesions reduced significantly during IFN beta. In session 1, patients demonstrated a greater between-run difference in functional MRI activity of secondary visual areas and cerebellum than controls. This abnormally large practice-induced signal change in visual areas, and in functionally connected posterior parietal and motor cortices, was reduced in patients in session 3 compared with 2. Our results suggest that MS inflammation alters short-term plasticity underlying motor practice. Reduction of inflammation with IFN beta is associated with a restoration of this plasticity, suggesting that modulation of inflammation may enhance recovery-oriented strategies that rely on patients' brain plasticity. Hum Brain Mapp 37:2431-2445, 2016. © 2016 Wiley Periodicals, Inc.
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http://dx.doi.org/10.1002/hbm.23184 | DOI Listing |
Langmuir
January 2025
Department of Physics and Astronomy, The University of Tennessee, Knoxville, Tennessee 37996, United States.
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January 2025
Vrije Universiteit Brussel, Brussels Health Centre, Brussels, Belgium.
Purpose: Cochlear implants (CI) are the most successful bioprosthesis in medicine probably due to the tonotopic anatomy of the auditory pathway and of course the brain plasticity. Correct placement of the CI arrays, respecting the inner ear anatomy are therefore important. The ideal trajectory to insert a cochlear implant array is defined by an entrance through the round window membrane and continues as long as possible parallel to the basal turn of the cochlea.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Biological Sciences, University of Southern California, 3616 Trousdale Parkway, AHF 252, Los Angeles, CA, 90089-0372, USA.
Habitual consumption of low-calorie sweeteners (LCS) during juvenile-adolescence can lead to greater sugar intake later in life. Here, we investigated if exposure to the LCS Acesulfame Potassium (Ace-K) during this critical period of development reprograms the taste system in a way that would alter hedonic responding for common dietary compounds. Results revealed that early-life LCS intake not only enhanced the avidity for a caloric sugar (fructose) when rats were in a state of caloric need, it increased acceptance of a bitterant (quinine) in Ace-K-exposed rats tested when middle-aged.
View Article and Find Full Text PDFTrends Neurosci
January 2025
Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA, USA. Electronic address:
Somatostatin-expressing (SST) neurons are a major class of electrophysiologically and morphologically distinct inhibitory cells in the mammalian neocortex. Transcriptomic data suggest that this class can be divided into multiple subtypes that are correlated with morpho-electric properties. At the same time, availability of transgenic tools to identify and record from SST neurons in awake, behaving mice has stimulated insights about their response properties and computational function.
View Article and Find Full Text PDFPharmacol Res
January 2025
Gill Institute for Neuroscience; Dept. of Psychological and Brain Sciences, Indiana University, Bloomington, IN 47405. Electronic address:
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