K Kato

Kochi University, Kôti, Kōchi, Japan

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Publications (15)115.01 Total impact

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    ABSTRACT: Post-traumatic stress disorder (PTSD) is a stress-related mental disorder caused by traumatic experience, and presents with characteristic symptoms, such as intrusive memories, a state of hyperarousal, and avoidance, that endure for years. Single-prolonged stress (SPS) is one of the animal models proposed for PTSD. Rats exposed to SPS showed enhanced inhibition of the hypothalamo-pituitary-adrenal (HPA) axis, which has been reliably reproduced in patients with PTSD, and increased expression of glucocorticoid receptor (GR) in the hippocampus. In this study, we characterized further neuroendocrinologic, behavioral and electrophysiological alterations in SPS rats. Plasma corticosterone recovered from an initial increase within a week, and gross histological changes and neuronal cell death were not observed in the hippocampus of the SPS rats. Behavioral analyses revealed that the SPS rats presented enhanced acoustic startle and impaired spatial memory that paralleled the deficits in hippocampal long-term potentiation (LTP) and depression. Contextual fear memory was enhanced in the rats 1 week after SPS exposure, whereas LTP in the amygdala was blunted. Interestingly, blockade of GR activation by administering 17-beta-hydroxy-11-beta-/4-/[methyl]-[1-methylethyl]aminophenyl/-17-alpha-[prop-1-ynyl]estra-4-9-diene-3-one (RU40555), a GR antagonist, prior to SPS exposure prevented potentiation of fear conditioning and impairment of LTP in the CA1 region. Altogether, SPS caused a number of behavioral changes similar to those described in PTSD, which marks SPS as a putative PTSD model. The preventive effects of a GR antagonist suggested that GR activation might play a critical role in producing the altered behavior and neuronal function of SPS rats.
    No preview · Article · Sep 2007 · Neuroscience
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    A. Hoshino · K. Kato · J. Takeuchi · H. Tsujino
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    ABSTRACT: In this paper, we describe development of an information service system using a humanoid robot. This system provides information such as topical news articles through conversations. Our goal is to evolve a conversational robot that can carry on conversations and enlighten the user. We think that achieving fun conversations is the basis for creating real symbiotic robots. This robot provides news information whether users explicitly ask for it or not during the conversation in order to attract users to conversations with the robot. The developed conversation mechanism is a natural extension of chatbot. Priorities for possible answers in response to user inputs are determined according to the dialogue strategy. This scheme is used for searching items from a news article database. With this method, one does not have to define an explicit domain model. This system can use pre-fixed databases but also renewable ones. We demonstrate the proposed idea on the humanoid robot, ASIMO.
    Full-text · Conference Paper · Sep 2005
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    ABSTRACT: To investigate the role in synaptic plasticity of Ca(2+) released from intracellular Ca(2+) stores, mice lacking the inositol 1,4,5-trisphosphate type 1 receptor were developed and the physiological properties, long-term potentiation, and long-term depression of their hippocampal CA1 neurons were examined. There were no significant differences in basic synaptic functions, such as membrane properties and the input/output relationship, between homozygote mutant and wild-type mice. Enhanced paired-pulse facilitation at interpulse intervals of less than 60 ms and enhanced post-tetanic potentiation were observed in the mutant mice, suggesting that the presynaptic mechanism was altered by the absence of the inositol 1,4,5-trisphosphate type 1 receptor. Long-term potentiation in the field-excitatory postsynaptic potentials induced by tetanus (100 Hz, 1 s) and the excitatory postsynaptic currents induced by paired stimulation in hippocampal CA1 pyramidal neurons under whole-cell clamp conditions were significantly greater in mutant mice than in wild-type mice. Homosynaptic long-term depression of CA1 synaptic responses induced by low-frequency stimulation (1 Hz, 500 pulses) was not significantly different, but heterosynaptic depression of the non-associated pathway induced by tetanus was blocked in the mutant mice. Both long-term potentiation and long-term depression in mutant mice were completely dependent on N-methyl-D-aspartate receptor activity. To rule out the possibility of an effect compensating for the lack of the inositol 1,4,5-trisphosphate type 1 receptor occurring during development, an anti-inositol 1,4,5-trisphosphate type 1 receptor monoclonal antibody that blocks receptor function was diffused into the wild-type cell through a patch pipette, and the effect of acute block of inositol 1,4,5-trisphosphate type 1 receptor on long-term potentiation was examined. Significant enhancement of long-term potentiation was observed compared with after control immunoglobulin G injection, suggesting that developmental redundancy was not responsible for the increase in long-term potentiation amplitude observed in the mutant mouse. The properties of channels that could be involved in long-term potentiation induction were examined using whole-cell recording. N-methyl-D-aspartate currents were significantly larger in mutant mice than in wild-type mice only between holding potentials of -60 and -80 mV. We conclude that inositol 1,4,5-trisphosphate type 1 receptor activity is not essential for the induction of synaptic plasticity in hippocampal CA1 neurons, but appears to negatively regulate long-term potentiation induction by mild modulation of channel activities.
    No preview · Article · Feb 2003 · Neuroscience
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    ABSTRACT: Protein tyrosine phosphatase delta (PTPdelta) is a receptor-type PTP expressed in the specialized regions of the brain including the hippocampal CA2 and CA3, B lymphocytes and thymic medulla. To elucidate the physiological roles of PTPdelta, PTPdelta-deficient mice were produced by gene targeting. It was found that PTPdelta-deficient mice were semi-lethal due to insufficient food intake. They also exhibited learning impairment in the Morris water maze, reinforced T-maze and radial arm maze tasks. Interestingly, although the histology of the hippocampus appeared normal, the magnitudes of long-term potentiation (LTP) induced at hippocampal CA1 and CA3 synapses were significantly enhanced in PTPdelta-deficient mice, with augmented paired-pulse facilitation in the CA1 region. Thus, it was shown that PTPdelta plays important roles in regulating hippocampal LTP and learning processes, and that hippocampal LTP does not necessarily positively correlate with spatial learning ability. To our knowledge, this is the first report of a specific PTP involved in the regulation of synaptic plasticity or in the processes regulating learning and memory.
    Full-text · Article · Jul 2000 · The EMBO Journal
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    ABSTRACT: Membrane potential recordings, made from the circular smooth muscle layer of the gastric antrum taken from mutant mice which lacked the inositol trisphosphate (InsP3) type 1 receptor, were compared with those obtained from the stomach of control (wild-type) mice. Immunostaining of gastric muscles indicated that the distribution and form of c-kit positive cells were similar in wild-type and mutant mice. Smooth muscles from wild-type mice generated slow waves that in turn initiated spike potentials, while those from mutant mice were either quiescent or generated irregular bursts of spike potentials. In the presence of nifedipine, slow waves with reduced amplitude were generated in wild-type mice, while all electrical activity was abolished in mutant mice. Acetylcholine depolarized and sodium nitroprusside hyperpolarized the membrane in muscles from both types of mice, being more effective in wild-type mice. Noradrenaline produced similar hyperpolarizations in both types of mice. Transmural nerve stimulation evoked inhibitory junction potentials (IJPs) in both wild-type and mutant mice. In wild-type mice, the IJPs were reduced in amplitude by nitroarginine and converted to a cholinergic excitatory junction potential (EJP) by apamin. In mutant mice, the IJPs were unaffected by nitroarginine or atropine but were abolished by apamin. It is concluded that in antral smooth muscle, the expression of InsP3 type 1 receptors may be causally related to the generation of slow waves but not to the generation of action potentials. A lack of InsP3 receptors attenuates cholinergic excitatory and nitrergic inhibitory responses but does not alter the response to noradrenaline.
    Full-text · Article · Jun 2000 · The Journal of Physiology
  • M. Nishiyama · K. Hong · K. Mikoshiba · M. Poo · K. Kato

    No preview · Article · Jan 2000 · Nature
  • K Kato · S T Li · C F Zorumski
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    ABSTRACT: We investigated mechanisms involved in the modulation of long-term potentiation by low concentrations of N-methyl-D-aspartate in the CA1 region of rat hippocampal slices. When applied for 5 min prior to and during tetanic stimulation, 1 microM N-methyl-D-aspartate inhibited long-term potentiation induction. Studies examining paired-pulse facilitation of non-N-methyl-D-aspartate receptor-mediated synaptic responses suggest that the effects of N-methyl-D-aspartate result in part from a presynaptic mechanism. This conclusion is supported by the observation that 1 microM N-methyl-D-aspartate failed to diminish N-methyl-D-aspartate receptor-mediated synaptic currents and that agents that enhance glutamate release, including high extracellular concentrations of calcium and an adenosine A1 receptor antagonist, overcome the long-term potentiation inhibition. Furthermore, the calcineurin inhibitors, FK-506 and cyclosporin A, as well as the phosphatase 1 and 2A inhibitor, okadaic acid, blocked the effects of N-methyl-D-aspartate on long-term potentiation suggesting a role for phosphatase activation in modulating the induction of long-term potentiation. These results show that the inhibition of long-term potentiation by untimely N-methyl-D-aspartate receptor activation is reversed by treatments that enhance glutamate release and suggest that adenosine release and diminished calcium influx during tetanic stimulation coupled with phosphatase activation contribute to the modulation of synaptic plasticity.
    No preview · Article · Feb 1999 · Neuroscience

  • No preview · Article · Jan 1999 · Journal of Neurochemistry
  • S.-T. Li · K. Kato · K. Mikoshiba

    No preview · Article · Dec 1998 · Neuroscience Research
  • K Takei · R M Shin · T Inoue · K Kato · K Mikoshiba
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    ABSTRACT: The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.
    No preview · Article · Dec 1998 · Science
  • K Kato · H Kato · K Mikoshiba

    No preview · Article · Oct 1998 · Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme
  • Kato K · Mikoshiba K

    No preview · Article · Dec 1996 · Neuroscience Research
  • K Kato · C F Zorumski
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    ABSTRACT: 1. The effects of the competitive nitric oxide (NO) synthase inhibitor, L-nitroarginine (L-NOArg), on synaptically activated N-methyl-D-aspartate (NMDA) currents and the induction of long-term potentiation (LTP) were studied in the CA1 region of rat hippocampal slices. 2. Application of 10 microM L-NOArg increased the amplitude of NMDA currents by approximately 50% in the presence of 2 mM extracellular Mg2+. This augmentation occurred within minutes of L-NOArg administration and was readily reversible on removal of the drug. L-arginine (100 microM) overcame the enhancement produced by L-NOArg. 3. At 5-100 microM, 10-25-min applications of L-NOArg facilitated the induction of LTP produced by a single 100 Hz X 300 ms tetanus. In control slices, the 100 Hz X 300 ms tetanus was insufficient to induce LTP. The development of LTP in L-NOArg-treated slices was inhibited by 50 microM D-2-amino-5-phosphonovalerate (D-APV), and the effects of L-NOArg were overcome by 10-fold higher concentrations of L-arginine but not by D-arginine. 4. Hemoglobin, an agent that binds NO extracellularly, also facilitated NMDA currents and the development of LTP when administered at 10 microM. 5. These results suggest that tonically released NO modulates the threshold for LTP in the CA1 hippocampal region and are consistent with prior studies indicating that untimely activation of NMDA receptors and release of NO inhibit LTP.
    No preview · Article · Oct 1993 · Journal of Neurophysiology
  • K Kato · D B Clifford · C F Zorumski
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    ABSTRACT: Factors involved in the production of long-term potentiation in the CA1 region of rat hippocampal slices were examined using whole-cell voltage clamp recordings. The pairing of postsynaptic membrane depolarization with tetanic stimulation produced a reliable long-lasting enhancement of synaptic currents provided that the pairing was performed within 15 min after establishing intracellular contact. This time could be extended to 30 min by including adenosine triphosphate and guanosine triphosphate in the recording pipette. Once established, the potentiation persisted for 3 h or more. The washout of long-term potentiation generating ability was not correlated with a rundown in baseline synaptic currents or in the N-methyl-D-aspartate receptor-mediated component of synaptic responses, but followed a time course similar to the loss of calcium spikes. Long-term potentiation could be reliably produced by depolarizing the postsynaptic membrane to -40 or -20 mV during the tetanus, but decreased when the membrane was held at membrane potentials greater than 0 mV. At -20 mV, 50 microM 2-amino-5-phosphonovalerate blocked the potentiation but this agent was ineffective at +40 mV. In contrast, 50 microM verapamil, a calcium channel blocker, failed to alter long-term potentiation at -20 mV but blocked the enhancement at +40 mV. These results suggest that whole-cell recording causes a washout of postsynaptic factors important in the initiation of long-term potentiation. However, these factors are less important in maintaining the potentiation. Furthermore, depending on the postsynaptic membrane potential during tetanic stimulation, voltage-gated calcium channels contribute to CA1 long-term potentiation.
    No preview · Article · Apr 1993 · Neuroscience
  • S.T. Li · K. Kato · K. Mikoshiba

    No preview · Article ·

Publication Stats

724 Citations
115.01 Total Impact Points

Institutions

  • 2007
    • Kochi University
      • Department of Neuropsychiatry
      Kôti, Kōchi, Japan
  • 2005
    • University of Tsukuba
      Tsukuba, Ibaraki, Japan
  • 2003
    • Kochi Medical School
      Kôti, Kōchi, Japan
  • 1999
    • RIKEN
      • Laboratory for Developmental Neurobiology
      Вако, Saitama, Japan
  • 1998-1999
    • Japan Science and Technology Agency (JST)
      Edo, Tōkyō, Japan
  • 1993
    • Washington University in St. Louis
      • Department of Psychiatry
      San Luis, Missouri, United States