Biology subjects

Kawase, S.

Publications and source records attributed to Kawase, S..

4 recordsLinked to original sources

bioRxiv2026

Differential physiological, behavioral, and medial prefrontal cortex transcriptomic responses to chronic restraint stress between BALB/c and C57BL/6J mice

Chronic stress is a major risk factor for psychiatric disorders such as depression and anxiety, yet the biological basis of individual differences in stress susceptibility and resilience remains poorly understood. Here, we examined physiological, behavioral, and medial prefrontal cortex (mPFC) transcriptomic responses to chronic restraint stress (CRS) in male BALB/c and C57BL/6J mice. After 21 days of CRS, BALB/c mice exhibited greater stress-related changes than C57BL/6J mice, including greater body weight loss, elevated serum corticosterone, reduced serum antioxidant capacity, and more pronounced depression-like behaviors. RNA sequencing showed largely strain-specific transcriptional changes in the mPFC. Strain x stress interaction analysis, followed by canonical pathway analysis using Ingenuity Pathway Analysis (IPA), identified strain-dependent molecular signatures. The most prominent differences involved extracellular matrix (ECM) organization and remodeling and neuroinflammatory signaling pathways, with greater predicted activation in BALB/c mice. IPA upstream regulator analysis further predicted multiple candidate regulators associated with these pathways, including TGF-{beta}/SMAD, C4a/C4b, and MAPK14. Among genes associated with these pathways, several ECM-related genes were preferentially upregulated in BALB/c mice, whereas activity-dependent immediate early genes were preferentially downregulated in C57BL/6J mice. These findings suggest that the strain-dependent mPFC transcriptional programs identified here may contribute to differential stress susceptibility and resilience.

neuroscience↗

bioRxiv2025

Century-old ethanol-preserved Vega Collection reveal the unexpected phylogeography of Slender bitterling Tanakia lanceolata in Japan

Recent genetic advancements offer new opportunities for studying natural history museum collections. The genetic analysis of century-old aquatic animal specimens, mostly preserved in ethanol, can provide valuable insights into the changes in genetic diversity caused by anthropogenic impacts. However, knowledge of the characteristics of degraded DNA from such specimens remains limited. In this study, we evaluated the DNA quality of bitterling fish, Tanakia lanceolata (Temminck and Schlegel), collected during the Vega Expedition in Japan in 1879 and preserved in ethanol. We then performed genomic analysis to test its hypothesized translocation-involved population history. The historical DNA was degraded, peaking around 50 bp, but a minor fraction exceeded 300 bp. Mitochondrial genetic analysis revealed high genetic similarity between the eastern and western sides of the Central Highland, typically impeding the dispersal of primary freshwater fish. These findings suggest an unexpected dispersal ability in T. lanceolata or undocumented translocations before the large-scale domestic translocations recorded since the 1910s. The customized workflow for historical ethanol-preserved specimens, based on historical DNA quality in this study, provides a foundation for studying historical archives.

evolutionary biology↗

bioRxiv2025

Intrathecal administration of palmitoyl-lysophosphatidylethanolamine reduces secondary injury and improves locomotor recovery following spinal cord injury

Spinal cord injury (SCI) triggers secondary pathophysiological cascades, including glutamate excitotoxicity, that result in neuronal loss and impair functional recovery. We have previously shown that lysophosphatidylethanolamine (LPE), a lysophospholipid, promotes neurite outgrowth and protects against glutamate excitotoxicity in cultured cortical neurons. However, whether these effects extend to spinal cord neurons and occur in vivo has remained unclear. In this study, we compared the effects of different LPE species: myristoyl-LPE (14:0 LPE), palmitoyl-LPE (16:0 LPE), stearoyl-LPE (18:0 LPE), and oleoyl-LPE (18:1 LPE) in cultured spinal commissural neurons, and evaluated their effects in vivo using a mouse model of SCI. In cultured neurons, all LPE species promoted neurite outgrowth. Although several species demonstrated a tendency toward neuroprotection, only 16:0 LPE exhibited a statistically significant protective effect against glutamate-induced excitotoxic cell death. Intrathecal administration of 16:0 LPE after SCI reduced TUNEL-positive cells in the acute phase and attenuated lesion expansion at 8 weeks post-injury. Moreover, 5-HT fluorescence intensity was increased in 16:0 LPE-treated mice, suggesting enhanced serotonergic innervation. Furthermore, administration of 16:0 LPE after SCI significantly improved hind-limb motor performance compared with vehicle controls, as assessed by the Basso Mouse Scale. Collectively, these findings suggest that intrathecal administration of 16:0 LPE reduces secondary injury and promotes functional recovery following SCI. Our findings highlight its potential as a therapeutic candidate for SCI.

neuroscience↗

bioRxiv2020

Neurexins play a crucial role in cerebellar granule cell survival by organizing autocrine machinery for neurotrophins

Neurexins (NRXNs) are among the key presynaptic cell adhesion molecules that regulate synapse function and formation via trans-synaptic interaction with postsynaptic ligands. Here, we generated cerebellar granule cell (CGC)-specific Nrxn triple-knockout (TKO) mice to allow the deletion of all NRXNs. Unexpectedly, most CGCs died in these mice. The requirement of NRNXs for cell survival was reproduced in cultured CGCs. We showed that the axons of cultured Nrxn TKO CGCs that were not in contact with the postsynaptic structure had defects in the formation of presynaptic protein cluster and action potential-induced Ca2+ influx. Additionally, these cells were impaired in the secretion from axons of depolarization-induced fluorescence-tagged brain-derived neurotrophic factor (BDNF), and the cell-survival defect was rescued by the application of BDNF. Our results suggest that CGC survival is maintained by autocrine neurotrophic factors, and that NRXNs organize the presynaptic protein clusters and the autocrine neurotrophic factor secretory machinery independent of contact with postsynaptic ligands.

neuroscience↗