Deploying and Optimizing Embodied Simulations of Large-Scale Spiking Neural Networks on HPC Infrastructure.

Simulating the brain-body-environment trinity in closed loop is an attractive proposal to investigate how perception, motor activity and interactions with the environment shape brain activity, and vice versa. The relevance of this embodied approach, however, hinges entirely on the modeled complexity of the various simulated phenomena. In this article, we introduce a software framework that is capable of simulating large-scale, biologically realistic networks of spiking neurons embodied in a biomechanically accurate musculoskeletal system that interacts with a physically realistic virtual environment.

Human-scale Brain Simulation via Supercomputer: A Case Study on the Cerebellum.

Performance of supercomputers has been steadily and exponentially increasing for the past 20 years, and is expected to increase further. This unprecedented computational power enables us to build and simulate large-scale neural network models composed of tens of billions of neurons and tens of trillions of synapses with detailed anatomical connections and realistic physiological parameters. Such "human-scale" brain simulation could be considered a milestone in computational neuroscience and even in general neuroscience.

Simulation of a Human-Scale Cerebellar Network Model on the K Computer.

Computer simulation of the human brain at an individual neuron resolution is an ultimate goal of computational neuroscience. The Japanese flagship supercomputer, K, provides unprecedented computational capability toward this goal. The cerebellum contains 80% of the neurons in the whole brain.

Large-Scale Simulation of a Layered Cortical Sheet of Spiking Network Model Using a Tile Partitioning Method.

One of the grand challenges for computational neuroscience and high-performance computing is computer simulation of a human-scale whole brain model with spiking neurons and synaptic plasticity using supercomputers. To achieve such a simulation, the target network model must be partitioned onto a number of computational nodes, and the sub-network models are executed in parallel while communicating spike information across different nodes. However, it remains unclear how the target network model should be partitioned for efficient computing on next generation of supercomputers.

Deficits in memory-guided limb movements impair obstacle avoidance locomotion in Alzheimer's disease mouse model.

Memory function deficits induced by Alzheimer's disease (AD) are believed to be one of the causes of an increased risk of tripping in patients. Working memory contributes to accurate stepping over obstacles during locomotion, and AD-induced deficits of this memory function may lead to an increased risk of contact with obstacles. We used the triple transgenic (3xTg) mice to examine the effects of memory deficits in terms of tripping and contact with obstacles.

Involvement of cholinergic system in hyperactivity in dopamine-deficient mice.

Dopaminergic systems have been known to be involved in the regulation of locomotor activity and development of psychosis. However, the observations that some Parkinson's disease patients can move effectively under appropriate conditions despite low dopamine levels (eg, kinesia paradoxia) and that several psychotic symptoms are typical antipsychotic resistant and atypical antipsychotic sensitive indicate that other systems beyond the dopaminergic system may also affect locomotor activity and psychosis. The present study showed that dopamine-deficient (DD) mice, which had received daily L-DOPA injections, could move effectively and even be hyperactive 72 h after the last L-DOPA injection when dopamine was almost completely depleted.

Ultrasound-enhanced delivery of morpholino with Bubble liposomes ameliorates the myotonia of myotonic dystrophy model mice.

Phosphorodiamidate morpholino oligonucleotide (PMO)-mediated control of the alternative splicing of the chloride channel 1 (CLCN1) gene is a promising treatment for myotonic dystrophy type 1 (DM1) because the abnormal splicing of this gene causes myotonia in patients with DM1. In this study, we optimised a PMO sequence to correct Clcn1 alternative splicing and successfully remedied the myotonic phenotype of a DM1 mouse model, the HSALR mouse. To enhance the efficiency of delivery of PMO into HSALR mouse muscles, Bubble liposomes, which have been used as a gene delivery tool, were applied with ultrasound exposure.

Characteristics of gait ataxia in δ2 glutamate receptor mutant mice, ho15J.

The cerebellum plays a fundamental, but as yet poorly understood, role in the control of locomotion. Recently, mice with gene mutations or knockouts have been used to investigate various aspects of cerebellar function with regard to locomotion. Although many of the mutant mice exhibit severe gait ataxia, kinematic analyses of limb movements have been performed in only a few cases.

Development of hand rehabilitation system for paralysis patient - universal design using wire-driven mechanism.

We have developed a hand rehabilitation system for patients suffering from paralysis or contracture. It consists of two components: a hand rehabilitation machine, which moves human finger joints with motors, and a data glove, which provides control of the movement of finger joints attached to the rehabilitation machine. The machine is based on the arm structure type of hand rehabilitation machine; a motor indirectly moves a finger joint via a closed four-link mechanism.

FraG is necessary for filament integrity and heterocyst maturation in the cyanobacterium Anabaena sp. strain PCC 7120.

Anabaena sp. strain PCC 7120 is a filamentous cyanobacterium that differentiates nitrogen-fixing heterocysts when fixed nitrogen becomes growth limiting in the medium. The gene alr2338 (designated fraG herein), located immediately upstream of the master regulator of differentiation hetR, was identified in a genetic screen for mutants unable to grow diazotrophically.