Integration of visual, vestibular, and proprioceptive sensations contributes to postural control. People with peripheral visual field loss have serious postural instability. However, the directional specificity of postural stability and sensory reweighting caused by gradual peripheral visual field loss remain unclear. What are the effects of peripheral visual field loss on static postural control? Fifteen healthy young adults participated in this study. The participants were asked to stand quietly on a foam surface. Three conditions of virtual visual field loss (90°, 45°, and 15°) were provided by a head-mounted display, and ground reaction forces were collected using a force plate to calculate the displacements of the center of pressure (COP). The root mean square (RMS), mean velocity, and 95% ellipse area of COP displacements in the horizontal plane increased, and RMS in the anteroposterior (AP) direction was unchanged under the smallest visual field condition compared to the largest one. The power spectrum density of COP displacements in the low-frequency band was decreased and that in the medium-frequency band was increased in the AP direction. During quiet standing of young healthy adults with peripheral visual field loss, increased peripheral visual field loss resulted in lower postural stability. Postural stability in the AP direction was maintained contrary to the functional sensitivity hypothesis. Peripheral visual field loss reduced the weighting of the visual input and increased that of the vestibular input in the AP direction to maintain equilibrium.

Magnetic fields are being used for detailed anatomical and functional examination of the human brain. In addition, evidences for their efficacy in treatment of brain dysfunctions is accumulating. Transcranial static magnetic field stimulation (tSMS) is a recently developed technique for non-invasively modifying brain functions. In tSMS, a strong and small magnet when placed over the skull can temporarily suppress brain functions. Its modulatory effects persist beyond the time of stimulation. However, the neurophysiological mechanisms underlying tSMS-induced plasticity remain unclear. Here, using acute motor cortical slice preparation obtained from male C57BL/6N mice, we show that tSMS alters the intrinsic electrical properties of neurons by altering the activity of chloride (Cl⁻) channels in neurons. Exposure of mouse pyramidal neurons to a static magnetic field (SMF) at a strength similar to human tSMS, temporarily decreased their excitability and induced transient neuronal swelling. The effects of SMF were blocked by DIDS and GlyH-101, but not by NPPB, consistent with the pharmacological profile of SLC26A11, a transporter protein with Cl⁻channel activity. Whole-cell voltage-clamp recordings of the GlyH-101-sensitive Cl⁻current component showed significant enhancement of the component at both subthreshold and depolarized membrane potentials after SMF application, resulting in shunting inhibition and reduced repetitive action potential (AP) firing at the respective potentials. Thus, this study provides the first neurophysiological evidence for the inhibitory effect of tSMS on neuronal activity and advances our mechanistic understanding of non-invasive human neuromodulation.Significance StatementTranscranial static magnetic field stimulation (tSMS) is a recently developed non-invasive brain stimulation technique. In tSMS, a strong, small magnet placed over the skull temporarily suppresses brain functions, and its modulatory effects persist beyond the stimulation time. To elucidate the neurophysiological mechanisms of tSMS, we evaluated the excitability of mouse pyramidal neurons exposed to a static magnetic field at a strength similar to that of human tSMS using whole-cell patch-clamp experiments. We demonstrated that the static magnetic field temporarily decreased neuronal excitability by increasing the activity of a specific type of Cl⁻channel in the plasma membrane, and it also induced transient neuronal swelling. This study reveals for the first time the neurophysiological mechanism of tSMS-induced suppression of brain functions.

Background. Due to the lack of effective therapies, stem cell transplantation is an anticipated treatment for chronic intracerebral hemorrhage (ICH), and higher cell survival and engraftment are considered to be the key for recovery. Mesenchymal stromal cells (MSCs) compounded with recombinant human collagen type I scaffolds (CellSaics) have a higher potential for cell survival and engraftment compared with solo-MSCs, and we investigated the validity of intracerebral transplantation of CellSaic in a chronic ICH model. Methods. Rat CellSaics (rCellSaics) were produced by rat bone marrow-derived MSC (rBMSCs). The secretion potential of neurotrophic factors and the cell proliferation rate were compared under oxygen-glucose deprivation (OGD) conditions. rCellSaics, rBMSCs, or saline were transplanted into the hollow cavity of a rat chronic ICH model. Functional and histological analyses were evaluated, and single-photon emission computed tomography for benzodiazepine receptors was performed to monitor sequential changes in neuronal integrity. Furthermore, human CellSaics (hCellSaics) were transplanted into a chronic ICH model in immunodeficient rats. Antibodies neutralizing brain-derived neurotrophic factor (BDNF) were used to elucidate its mode of action. Results. rCellSaics demonstrated a higher secretion potential of trophic factors and showed better cell proliferation in the OGD condition. Animals receiving rCellSaics displayed better neurological recovery, higher intracerebral BDNF, and better cell engraftment; they also showed a tendency for less brain atrophy and higher benzodiazepine receptor preservation. hCellSaics also promoted significant functional recovery, which was reversed by BDNF neutralization. Conclusion. Intracerebral transplantation of CellSaics enabled neurological recovery in a chronic ICH model and may be a good option for clinical application.