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A frontal transcallosal inhibition loop mediates interhemispheric balance in visuospatial processing.
Nat Commun
August 2023
Songjiang Research Institute, Shanghai Songjiang District Central Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200025, China.
Interhemispheric communication through the corpus callosum is required for both sensory and cognitive processes. Impaired transcallosal inhibition causing interhemispheric imbalance is believed to underlie visuospatial bias after frontoparietal cortical damage, but the synaptic circuits involved remain largely unknown. Here, we show that lesions in the mouse anterior cingulate area (ACA) cause severe visuospatial bias mediated by a transcallosal inhibition loop.
View Article and Find Full Text PDFDo Adults with Stroke have Altered Interhemispheric Inhibition? A Systematic Review with Meta-Analysis.
J Stroke Cerebrovasc Dis
July 2022
Innovation, Implementation and Clinical Translation (IIMPACT) in Health, Allied Health and Human Performance, University of South Australia, North Terrace, Adelaide 5000, Australia; Brain Stimulation, Imaging and Cognition Research Group, School of Biomedicine, The University of Adelaide, North Tce, Adelaide 5005, Australia.
Objective: Interhemispheric inhibition is an important cortical mechanism to support motor control. Altered interhemispheric inhibition has been the target of neuromodulation interventions. This systematic review investigated the evidence for altered interhemispheric inhibition in adults with unilateral neurological conditions: stroke, amyotrophic lateral sclerosis, cerebral palsy, complex regional pain syndrome, traumatic brain injury, and cerebral palsy METHODS: We pre-registered the protocol and followed PRISMA guidelines.
View Article and Find Full Text PDFReversible splenial lesion syndrome in sisters with sensorineural deafness as the first manifestation.
Heliyon
May 2021
Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Reversible splenial lesion syndrome (RESLES) is a rare clinico-radiological disorder syndrome with unclear pathophysiology. Here, two sisters with sensorineural deafness as the chief complaint diagnosed with RESLES was reported. Although the sisters had the disease successively, they were divided into two types on imaging by isolated lesions of splenium of the corpus callosum (SCC) and extensive lesions of the corpus callosum.
View Article and Find Full Text PDFActivity in grafted human iPS cell-derived cortical neurons integrated in stroke-injured rat brain regulates motor behavior.
Proc Natl Acad Sci U S A
April 2020
Laboratory of Stem Cells and Restorative Neurology, Lund Stem Cell Center, Lund University, SE-22184 Lund, Sweden;
Stem cell transplantation can improve behavioral recovery after stroke in animal models but whether stem cell-derived neurons become functionally integrated into stroke-injured brain circuitry is poorly understood. Here we show that intracortically grafted human induced pluripotent stem (iPS) cell-derived cortical neurons send widespread axonal projections to both hemispheres of rats with ischemic lesions in the cerebral cortex. Using rabies virus-based transsynaptic tracing, we find that at 6 mo after transplantation, host neurons in the contralateral somatosensory cortex receive monosynaptic inputs from grafted neurons.
View Article and Find Full Text PDFIn vivo epigenetic editing of Sema6a promoter reverses transcallosal dysconnectivity caused by C11orf46/Arl14ep risk gene.
Nat Commun
September 2019
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Many neuropsychiatric risk genes contribute to epigenetic regulation but little is known about specific chromatin-associated mechanisms governing the formation of neuronal connectivity. Here we show that transcallosal connectivity is critically dependent on C11orf46, a nuclear protein encoded in the chromosome 11p13 WAGR risk locus. C11orf46 haploinsufficiency was associated with hypoplasia of the corpus callosum.
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