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Holding still and aiming reaches to spatial targets may depend on distinct neural circuits. Using automated homecage training and a sensitive joystick, we trained freely moving mice to contact a joystick, hold their forelimb still, and then reach to rewarded target locations. Mice learned the task by initiating forelimb sequences with clearly resolved submillimeter-scale micromovements followed by millimeter-scale reaches to learned spatial targets. Hundreds of thousands of trajectories were decomposed into millions of kinematic submovements, while photoinhibition was used to test roles of motor cortical areas. Inactivation of both caudal and rostral forelimb areas preserved the ability to produce aimed reaches, but reduced reach speed. Inactivation specifically of contralateral caudal forelimb area (CFA) additionally impaired the ability to aim corrective submovements to remembered locations following target undershoots. Our findings show that motor cortical inactivations reduce the gain of forelimb movements but that inactivation specifically of contralateral CFA impairs corrective movements important for reaching a target location. To test the role of different cortical areas in holding still and reaching to targets, this study combined home-cage training with optogenetic silencing as mice engaged in a learned center-out-reach task. Inactivation specifically of contralateral caudal forelimb area (CFA) impaired corrective movements necessary to reach spatial targets to earn reward.
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http://dx.doi.org/10.1152/jn.00241.2023 | DOI Listing |
Neurobiol Dis
December 2024
Graduate Institute of Brain and Mind Sciences, National Taiwan University College of Medicine, Taipei 10051, Taiwan. Electronic address:
Evidence indicates that neurodegenerative diseases spread through distinct brain networks. For Parkinson's disease (PD), somatosensory abnormalities may accompany motor dysfunction in early disease stages when dopaminergic degeneration is limited to the basal ganglia. It remains unclear whether, based on the network-spread account, these abnormalities emanated from aberrant functional connectivity with the basal ganglia, and whether interventions normalizing this connectivity could reverse these abnormalities.
View Article and Find Full Text PDFEpilepsia Open
December 2024
Integrated Diagnostics for Epilepsy, Department of Diagnostic and Technology, European Reference Network EPIcare, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
Neuronal ceroid lipofuscinoses (NCLs) are genetically heterogeneous neurodegenerative disorders, characterized by progressive cognitive and motor decline, epilepsy, visual impairment, and shortened life-expectancy. CLN6-related NCLs include both late-infantile and adult myoclonic form. We report a 21-year-old patient, with mild developmental delay, who developed occipital seizures at 14 years, and subsequently cognitive decline, cortical myoclonus, and photosensitivity at low and higher frequencies.
View Article and Find Full Text PDFBrain Struct Funct
December 2024
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Aim: To describe the cortical brain development and full-IQ performance in middle school age children after extremely preterm (EPT) birth considering discrete white matter abnormalities (WMA). In addition, to assess possible early motor predictors of cortical brain development and full-IQ in children born EPT with and without discrete WMA diagnosed at 10 years.
Methods: T1-weighted MRI images from fifty-one children born before 27 weeks' gestation and 40 full-term born controls (M=10.
Cureus
November 2024
Department of Surgery - Center for Anatomical Science and Education, Saint Louis University School of Medicine, St. Louis, USA.
Polymicrogyria (PMG) is the most common malformation of cortical development (MCD) and presents as an irregularly patterned cortical surface with numerous small gyri and shallow sulci leading to various neurological deficits including developmental delays, intellectual disability, epilepsy, and language and motor issues. The presentation of PMG varies and is often found in conjunction with other congenital anomalies. Histologically, PMG features an abnormal cortical structure and dyslamination, resulting in its classification as a defect of neuronal migration and organization.
View Article and Find Full Text PDFJ Neurosci Res
December 2024
National Center for Drug Research and Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Niemann Pick type C1 (NPC1) is a rare, fatal disorder characterized by endosomal lipid accumulation that leads to damage of both peripheral organs and central nervous system (cerebellum and hippocampus are especially affected). Currently, miglustat is the only approved drug for NPC1, thus the identification of new treatments is mandatory. We have previously demonstrated that the drug dipyridamole (DIP), an enhancer of adenosine signaling, can reduce the pathological phenotype in patient-derived fibroblasts.
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