The University of Osaka · Neuroscience
Professor Takahide Itokazu's research lab focuses on the neural mechanisms underlying neurological disorders, with a central emphasis on neuroinflammation, axon regeneration, and neural circuitry in conditions such as stroke, multiple sclerosis, and spinal cord injury. The lab investigates key molecular players like RGMa and IL-17A in glial cell responses and neural repair, utilizing advanced techniques including optogenetics, in vivo imaging, and genetic manipulation in mouse models. A major research direction involves identifying therapeutic targets—such as microglia and ependymal cells—for neuropathic pain and functional recovery after CNS injury. The lab also explores biomarkers and neuroimaging correlates to evaluate treatment efficacy in real time.
Figures are computed from collected data and may differ slightly.
Cortical computation is distributed across multiple areas of the cortex by networks of reciprocal connectivity. However, how such connectivity contributes to the communication between the connected areas is not clear. In this study, we examine the communication between sensory and motor cortices. We develop an eye movement task in mice and combine it with optogenetic suppression and two-photon calcium imaging techniques. We identify a small region in the secondary motor cortex (MO<sub>s</sub>) t
Central poststroke pain (CPSP) is one of the neuropathic pain syndromes that can occur following stroke involving the somatosensory system. However, the underlying mechanism of CPSP remains largely unknown. Here, we established a CPSP mouse model by inducing a focal hemorrhage in the thalamic ventrobasal complex and confirmed the development of mechanical allodynia. In this model, microglial activation was observed in the somatosensory cortex, as well as in the injured thalamus. By using a CSF1
RGMa signaling in infiltrated macrophages is a critical driver of neutrophil-related astrocytopathy in NMO lesions, and RGMa-mAb may provide an efficient therapeutic strategy for NMO-associated neuropathic pain and motor deficits in patients with NMO. ANN NEUROL 2022;91:532-547.
Ependymal cells have been suggested to act as neural stem cells and exert beneficial effects after spinal cord injury (SCI). However, the molecular mechanism underlying ependymal cell regulation after SCI remains unknown. To examine the possible effect of IL-17A on ependymal cell proliferation after SCI, we locally administrated IL-17A neutralizing antibody to the injured spinal cord of a contusion SCI mouse model, and revealed that IL-17A neutralization promoted ependymal cell proliferation, wh
Repulsive guidance molecule (RGM) is a membrane-bound protein that was originally identified as an axon guidance molecule in the chick retinotectal system. RGMa, one of the 3 isoforms found in mammals, is involved in laminar patterning, cephalic neural tube closure, axon guidance, and inhibition of axonal regeneration. In addition to its roles in the nervous system, RGMa plays a role in enhancing helper T-cell activation. Binding of RGM to its receptor, neogenin, is considered necessary to trans
The lack of established biomarkers which reflect dynamic neuropathological alterations in multiple sclerosis (MS) makes it difficult to determine the therapeutic response to the tested drugs and to identify the key biological process that mediates the beneficial effect of them. In the present study, we applied high-field MR imaging in locally-induced experimental autoimmune encephalomyelitis (EAE) mice to evaluate dynamic changes following treatment with a humanized anti-repulsive guidance molec
We conclude that mesocortical dopamine axon terminals encode the timing of self-initiated actions, shedding light on a crucial aspect of the intricate neural mechanisms governing goal-directed behavior.
Cognitive impairment is a significant complication of diabetes. Although the detailed mechanism remains unclear, prolonged neuroinflammation mediated by microglia is recognized as a key contributor to neural dysfunction. Recent studies have shown that Formyl peptide receptor 1 (FPR1), a G protein-coupled chemoattractant receptor, plays a role in microglial activation and brain pathology. However, the involvement of FPR2, another isoform within the FPR family, in microglial activation and cogniti
Brachial plexus injury is a neurological injury caused by trauma, and effective treatments remain limited. Understanding its pathology is necessary to develop new therapeutic strategies. In this study, we used a dorsal root avulsion mouse model to determine whether injury-induced alterations in feedback circuitry from the dorsal root ganglion (DRG) to motor neurons contribute to functional recovery. We visualized axons originating from DRG neurons by directly injecting adeno-associated virus enc
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