Publications by authors named "Keiko Karasawa"

The biological activities of substances in the brain are shaped by their spatiotemporal dynamics in brain tissues, all of which are regulated by water dynamics. In contrast to solute dynamics, water dynamics have been poorly characterized, owing to the lack of appropriate analytical tools. To overcome this limitation, we apply stimulated Raman scattering multimodal multiphoton microscopy to live brain tissues.

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Article Synopsis
  • Oxytocin's role and mechanisms in the brain are not well understood, prompting the development of a new oxytocin analogue probe using a simple alkyne coupling reaction for better study.
  • The alkyne-tagged oxytocin displays similar behavior to natural oxytocin while enabling precise detection in brain tissue, revealing high-affinity binding sites in the hippocampus.
  • This technique not only clarifies oxytocin's dynamics and transmission in the brain but is also useful for investigating other small peptides, advancing our understanding of central peptide signaling.
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Observing multiple molecular species simultaneously with high spatiotemporal resolution is crucial for comprehensive understanding of complex, dynamic, and heterogeneous biological systems. The recently reported super-multiplex optical imaging breaks the "color barrier" of fluorescence to achieve multiplexing number over six in living systems, while its temporal resolution is limited to several minutes mainly by slow color tuning. Herein, we report integrated stimulated Raman and fluorescence microscopy with simultaneous multimodal color tunability at high speed, enabling super-multiplex imaging covering diverse molecular contrasts with temporal resolution of seconds.

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The dopaminergic system is essential for the function of the brain in health and disease. Therefore, detailed studies focused on unraveling the mechanisms involved in dopaminergic signaling are required. However, the lack of probes that mimic dopamine in living tissues, owing to the neurotransmitter's small size, has hampered analysis of the dopaminergic system.

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Brn4, which encodes a POU transcription factor, is the gene responsible for DFN3, an X chromosome-linked, non-syndromic type of hearing loss. Brn4-deficient mice have a low endocochlear potential (EP), hearing loss, and ultrastructural alterations in spiral ligament fibrocytes, however the molecular pathology through which Brn4 deficiency causes low EP is still unclear. Mutations in the Gjb2 and Gjb6 genes encoding the gap junction proteins connexin26 (Cx26) and connexin30 (Cx30) genes, respectively, which encode gap junction proteins and are expressed in cochlear fibrocytes and non-sensory epithelial cells (i.

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Article Synopsis
  • Hereditary deafness affects about 1 in 2,000 children, often due to mutations in the gene for the cochlear gap junction protein connexin 26 (CX26), which accounts for 50% of cases in some populations.
  • CX26 deficiency disrupts the development of the auditory sensory epithelium and is not compensated by the similar connexin CX30, even though both are present in cochlear cells.
  • In mouse models, researchers found that loss of CX26 leads to early changes during embryonic development, including a reduction in gap junction plaques and increased endocytosis, highlighting a link between CX26 mutations and the degeneration of gap junction complexes.
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Background: The greater epithelial ridge (GER) is a developmental structure in the maturation of the organ of Corti. Situated near the inner hair cells of neonatal mice, the GER undergoes a wave of apoptosis after postnatal day 8 (P8). We evaluated the GER from P8 to P12 in transgenic mice that carry the R75W + mutation, a dominant-negative mutation of human gap junction protein, beta 2, 26 kDa (GJB2) (also known as connexin 26 or CX26).

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