Tatsuya Mishima

Summary

Affiliation: Kyorin University
Country: Japan

Publications

  1. ncbi Reduction of neurotransmitter release by the exogenous H3 domain peptide of HPC-1/syntaxin 1A in cultured rat hippocampal neurons
    Tatsuya Mishima
    Department of Physiology, Kyorin University School of Medicine, Shinkawa 6 20 2, Mitaka, Tokyo 181 8611, Japan
    Neurosci Lett 329:273-6. 2002
  2. doi HPC-1/syntaxin 1A and syntaxin 1B play distinct roles in neuronal survival
    Takefumi Kofuji
    Radioisotope Laboratory, Kyorin University School of Medicine, Mitaka, Tokyo, Japan
    J Neurochem 130:514-25. 2014
  3. doi Impairment of catecholamine systems during induction of long-term potentiation at hippocampal CA1 synapses in HPC-1/syntaxin 1A knock-out mice
    Tatsuya Mishima
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo 181 8611, Japan
    J Neurosci 32:381-9. 2012
  4. ncbi Analysis of knock-out mice to determine the role of HPC-1/syntaxin 1A in expressing synaptic plasticity
    Tomonori Fujiwara
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo 181 8611, Japan
    J Neurosci 26:5767-76. 2006
  5. pmc Syntaxin 1B, but not syntaxin 1A, is necessary for the regulation of synaptic vesicle exocytosis and of the readily releasable pool at central synapses
    Tatsuya Mishima
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo, Japan
    PLoS ONE 9:e90004. 2014
  6. doi Calcium loading capacity and morphological changes in mitochondria in an ischemic preconditioned model
    Takehiko Iijima
    Department of Anesthesiology, Kyorin University, School of Medicine, Japan
    Neurosci Lett 448:268-72. 2008
  7. ncbi Neuroprotective effect of propofol on necrosis and apoptosis following oxygen-glucose deprivation--relationship between mitochondrial membrane potential and mode of death
    Takehiko Iijima
    Department of Anesthesiology, Kyorin University, School of Medicine, Tokyo, Japan
    Brain Res 1099:25-32. 2006
  8. ncbi Mitochondrial membrane potential and intracellular ATP content after transient experimental ischemia in the cultured hippocampal neuron
    Takehiko Iijima
    Department of Anesthesiology, School of Medicine, Kyorin University, 6 20 2 Shinkawa, Mitaka City, Tokyo 181, Japan
    Neurochem Int 43:263-9. 2003
  9. ncbi Mitochondrial hyperpolarization after transient oxygen-glucose deprivation and subsequent apoptosis in cultured rat hippocampal neurons
    Takehiko Iijima
    Department of Anesthesiology, Kyorin University School of Medicine, 6 20 2 Shinkawa, Mitaka City 181 8611, Tokyo, Japan
    Brain Res 993:140-5. 2003
  10. doi ER and Golgi stresses increase ER-Golgi SNARE Syntaxin5: Implications for organelle stress and βAPP processing
    Kei Suga
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo 181 8611, Japan Electronic address
    Neurosci Lett 604:30-5. 2015

Collaborators

Detail Information

Publications10

  1. ncbi Reduction of neurotransmitter release by the exogenous H3 domain peptide of HPC-1/syntaxin 1A in cultured rat hippocampal neurons
    Tatsuya Mishima
    Department of Physiology, Kyorin University School of Medicine, Shinkawa 6 20 2, Mitaka, Tokyo 181 8611, Japan
    Neurosci Lett 329:273-6. 2002
    ..These results suggest that the H3 domain peptide reduces neurotransmitter release by retarding the refilling of readily releasable vesicles...
  2. doi HPC-1/syntaxin 1A and syntaxin 1B play distinct roles in neuronal survival
    Takefumi Kofuji
    Radioisotope Laboratory, Kyorin University School of Medicine, Mitaka, Tokyo, Japan
    J Neurochem 130:514-25. 2014
    ..STX1B was important for neuronal survival, possibly by regulating the secretion of neurotrophic factors, such as BDNF, from glial cells. ..
  3. doi Impairment of catecholamine systems during induction of long-term potentiation at hippocampal CA1 synapses in HPC-1/syntaxin 1A knock-out mice
    Tatsuya Mishima
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo 181 8611, Japan
    J Neurosci 32:381-9. 2012
    ..Theses results suggest that HPC-1/syntaxin 1A regulates catecholaminergic systems via exocytosis of dense-core synaptic vesicles, and that deletion of HPC-1/syntaxin 1A causes impairment of LTP induction...
  4. ncbi Analysis of knock-out mice to determine the role of HPC-1/syntaxin 1A in expressing synaptic plasticity
    Tomonori Fujiwara
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo 181 8611, Japan
    J Neurosci 26:5767-76. 2006
    ..Interestingly, the KO mice had impaired conditioned fear memory extinction. These observations suggest that HPC-1/syntaxin 1A may be closely related to synaptic plasticity...
  5. pmc Syntaxin 1B, but not syntaxin 1A, is necessary for the regulation of synaptic vesicle exocytosis and of the readily releasable pool at central synapses
    Tatsuya Mishima
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo, Japan
    PLoS ONE 9:e90004. 2014
    ..Our results suggest that although STX1A and 1B share a basic function as neuronal t-SNAREs, STX1B but not STX1A is necessary for the regulation of spontaneous and evoked synaptic vesicle exocytosis in fast transmission. ..
  6. doi Calcium loading capacity and morphological changes in mitochondria in an ischemic preconditioned model
    Takehiko Iijima
    Department of Anesthesiology, Kyorin University, School of Medicine, Japan
    Neurosci Lett 448:268-72. 2008
    ..Our observations suggest that subpopulations of mitochondria with specific morphologies are linked to the CLC and mPT...
  7. ncbi Neuroprotective effect of propofol on necrosis and apoptosis following oxygen-glucose deprivation--relationship between mitochondrial membrane potential and mode of death
    Takehiko Iijima
    Department of Anesthesiology, Kyorin University, School of Medicine, Tokyo, Japan
    Brain Res 1099:25-32. 2006
    ..Propofol induces a moratorium on neuronal death, during which pharmacological intervention might be able to prevent cell death...
  8. ncbi Mitochondrial membrane potential and intracellular ATP content after transient experimental ischemia in the cultured hippocampal neuron
    Takehiko Iijima
    Department of Anesthesiology, School of Medicine, Kyorin University, 6 20 2 Shinkawa, Mitaka City, Tokyo 181, Japan
    Neurochem Int 43:263-9. 2003
    ..This pathological finding of an energy-producing system after OGD may provide a clue to explain post-ischemic energy failure...
  9. ncbi Mitochondrial hyperpolarization after transient oxygen-glucose deprivation and subsequent apoptosis in cultured rat hippocampal neurons
    Takehiko Iijima
    Department of Anesthesiology, Kyorin University School of Medicine, 6 20 2 Shinkawa, Mitaka City 181 8611, Tokyo, Japan
    Brain Res 993:140-5. 2003
    ..Neurons were still viable even during hyperpolarization of mitochondria, but this hyperpolarization appears to be linked to subsequent apoptotic change...
  10. doi ER and Golgi stresses increase ER-Golgi SNARE Syntaxin5: Implications for organelle stress and βAPP processing
    Kei Suga
    Department of Cell Physiology, Kyorin University School of Medicine, Mitaka, Tokyo 181 8611, Japan Electronic address
    Neurosci Lett 604:30-5. 2015
    ..These findings suggest that Syx5 is a potential stress responsive factor that participates in βAPP processing and the survival pathways of neuronal cells. ..