Biology subjects

Ichiyama, R. M.

Publications and source records attributed to Ichiyama, R. M..

3 recordsLinked to original sources

bioRxiv2025

Exercise remodels hippocampal extracellular matrix to alleviate chondroitin-4-sulphate-induced memory impairment.

Research utilising exercise therapeutically to enhance neuroplasticity mainly reports enhanced expression of neurotrophic (neural growth) factors which are associated with increased neurogenesis, structural changes, and improved memory. However, these neural changes are tightly regulated by both promotors and inhibitors of neuroplasticity, and the effect of exercise on inhibitory pathways is currently understudied. We show that exercise also modulates inhibitors of neuroplasticity. Six weeks of treadmill training reduced the gene expression of aggrecan, a chondroitin sulphate proteoglycan (CSPG), and altered the composition of CSPG containing structures, perineuronal nets, in the rodent hippocampus. Genetically manipulating chondroitin-4-sulphation of CSPGs by overexpressing hippocampal Chst11 impaired memory performance, which was mitigated by treadmill training. We provide evidence that hippocampal CSPGs are involved in object recognition memory, and that there is a link between exercise, modulating hippocampal inhibitors of neuroplasticity, and memory performance.

neuroscience↗

bioRxiv2023

Spinal facilitation of descending motor input

Highly varying patterns of electrostimulation (Dynamic Stimulation, DS) delivered to the dorsal cord through an epidural array with 18 independent electrodes transiently facilitate corticospinal motor responses, even after spinal injury. To partly unravel how corticospinal input are affected by DS, we introduced a corticospinal platform that allows selective cortical stimulation during the multisite acquisition of cord dorsum potentials (CDPs) and the simultaneous supply of DS. Firstly, the epidural interface was validated by the acquisition of the classical multisite distribution of CDPs on the dorsal cord and their input-output profile elicited by pulses delivered to peripheral nerves. Apart from increased EMGs, DS selectively increased excitability of the spinal interneurons that first process corticospinal input, without changing the magnitude of commands descending from the motor cortex, suggesting a novel correlation between muscle recruitment and components of cortically-evoked CDPs. Finally, DS increases excitability of post-synaptic spinal interneurons at the stimulation site and their responsiveness to any residual supraspinal control, thus supporting the use of electrical neuromodulation whenever the motor output is jeopardized by a weak volitional input, due to a partial disconnection from supraspinal structures and/or neuronal brain dysfunctions.

neuroscience↗

bioRxiv2020

Caudal-rostral progression of alpha motoneurone degeneration in the SOD1G93A mouse model of amyotrophic lateral sclerosis

Mice with transgenic expression of human SOD1G93A are a widely used model of ALS, with a caudal-rostral progression of motor impairment. Previous studies have quantified the progression of motoneurone (MN) degeneration based on size, even though alpha (-) and gamma ({gamma}-) MNs overlap in size. Therefore, using molecular markers and synaptic inputs, we quantified the survival of -MNs and {gamma}-MNs at the lumbar and cervical spinal segments of 3- and 4-month SOD1G93A mice, to investigate whether there is a caudal-rostral progression of MN death. By 3-months, in the cervical and lumbar spinal cord, there was -MN degeneration with complete {gamma}-MN sparing. At 3-months the cervical spinal cord had more -MNs per ventral horn than the lumbar spinal cord, in SOD1G93A mice. A similar spatial trend of degeneration was observed in the corticospinal tract, which remained intact in the cervical spinal cord at 3- and 4-months of age. These findings agree with the corticofugal synaptopathy model, that -MN and CST of the lumbar spinal cord are more susceptible to degeneration in SOD1G93A mice. Hence, there is spatial and temporal caudal-rostral progression of -MN and CST degeneration in SOD1G93A mice. HighlightsO_LISOD1G93A mice display a caudal-rostral progression of motor impairment. C_LIO_LILumbar spinal cord of SOD1G93A mice has an enhanced susceptibility to degeneration. C_LIO_LISOD1G93A mice exhibit a caudal-rostral progression of -MN and CST degeneration C_LI

neuroscience↗