K Kato

Kochi University, Kôti, Kōchi, Japan

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Publications (14)143.11 Total impact

  • [Show abstract] [Hide abstract]
    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.
    Neuroscience 09/2007; 148(1):22-33. · 3.12 Impact Factor
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    ABSTRACT: This paper presents a new type of conversational humanoid robot, which can engage in both task-oriented dialogues and non-task-oriented dialogues. Most previously built conversational robots can engage in either task-oriented dialogues for accurately understanding human requests or non-task-oriented dialogues to allow humans to enjoy conversations. Since both are beneficial functionalities for a humanoid robot as a human partner, it is desirable for one humanoid robot to be able to engage in both types of dialogues. Our model is based on a multi-expert model, which features control modules called experts each of which is specialized to perform certain kinds of tasks through performing physical actions and engaging in dialogues. One of the experts takes charge in understanding human utterances and deciding robot utterances or actions. Non-task-oriented dialogue functionality is incorporated into this model by building an expert called the chat expert which is dedicated to non-task-oriented dialogues. The chat expert utilizes the outputs of a large-vocabulary speech recognizer, while other task-oriented experts utilize the outputs of a small-vocabulary speech recognizer. By selecting an appropriate expert according to the speech recognition result and dialogue context, we can alleviate degradation in speech recognition accuracy in spite of incorporating a large-vocabulary speech recognizer. The chat expert is dealt with as the default expert that has the responsibility to reply to human utterances. If a human utterance is considered to be a request for a task with a high plausibility, the expert for understanding the request is selected. The implemented system, which has been combined with Honda ASIMO, demonstrates that it can dynamically change dialogue strategy based on speech recognition results
    Humanoid Robots, 2006 6th IEEE-RAS International Conference on; 01/2007
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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.
    Robot and Human Interactive Communication, 2005. ROMAN 2005. IEEE International Workshop on; 09/2005
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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.
    Neuroscience 02/2003; 117(4):821-30. · 3.12 Impact Factor
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    ABSTRACT: Short-term plasticity, the effect of a preceding synaptic response on the following response in a pair, in layers II/III of the rat auditory cortex slice after application of repetitive stimuli to layer IV, was investigated using a multichannel extracellular recording system. Paired-pulse depression, which is induced to a moderate degree in standard artificial cerebrospinal fluid, was markedly facilitated in the presence of bicuculline, a GABA(A) receptor antagonist, concurrent with the emergence of a polysynaptic component of the EPSP (polyEPSP) in the first response in a pair. This depression (bicuculline-facilitated synaptic depression, BFSD) was maximal at the minimum interval tested (50 ms), reduced as the interval was increased, and persisted beyond an interval of 2 s. The occurrence of BFSD was dependent on the presence of a polyEPSP regardless of the presence of the monosynaptic component of the EPSP, indicating that BFSD is induced by a heterosynaptic mechanism. D-AP5, an NMDA receptor antagonist, partially eliminated polyEPSPs and reversed BFSD. These results suggest that activation of polysynaptic excitatory pathways induces a heterosynaptic depression in the range of a few seconds and that NMDA receptor activity is involved in this heterosynaptic depression.
    Neuroscience Research 06/2001; 40(1):67-74. · 2.20 Impact Factor
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    ABSTRACT: Activity-induced synaptic modification is essential for the development and plasticity of the nervous system. Repetitive correlated activation of pre- and postsynaptic neurons can induce persistent enhancement or decrement of synaptic efficacy, commonly referred to as long-term potentiation or depression (LTP or LTD). An important unresolved issue is whether and to what extent LTP and LTD are restricted to the activated synapses. Here we show that, in the CA1 region of the hippocampus, reduction of postsynaptic calcium influx by partial blockade of NMDA (N-methyl-D-aspartate) receptors results in a conversion of LTP to LTD and a loss of input specificity normally associated with LTP, with LTD appearing at heterosynaptic inputs. The induction of LTD at homo- and heterosynaptic sites requires functional ryanodine receptors and inositol triphosphate (InsP3) receptors, respectively. Functional blockade or genetic deletion of type 1 InsP3 receptors led to a conversion of LTD to LTP and elimination of heterosynaptic LTD, whereas blocking ryanodine receptors eliminated only homosynaptic LTD. Thus, postsynaptic Ca2+, deriving from Ca2+ influx and differential release of Ca2+ from internal stores through ryanodine and InsP3 receptors, regulates both the polarity and input specificity of activity-induced synaptic modification.
    Nature 12/2000; 408(6812):584-8. · 38.60 Impact Factor
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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.
    The EMBO Journal 07/2000; 19(12):2775-85. · 9.82 Impact Factor
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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.
    The Journal of Physiology 06/2000; 525 Pt 1:105-11. · 4.38 Impact Factor
  • Nature 01/2000; · 38.60 Impact Factor
  • 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.
    Neuroscience 02/1999; 92(4):1261-72. · 3.12 Impact Factor
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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.
    Science 12/1998; 282(5394):1705-8. · 31.03 Impact Factor
  • K Kato, H Kato, K Mikoshiba
    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme 10/1998; 43(12 Suppl):1561-6.
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    ABSTRACT: The inositol 1,4,5-trisphosphate receptor (InsP3R) is an intracellular Ca2+ channel that releases Ca2+ from internal Ca2+ stores in response to InsP3. Although InsP3R is highly expressed in various regions of the mammalian brain, the functional role of this receptor has not been clarified. We show here that cerebellar slices prepared from mice with a disrupted InsP3R type 1 gene, which is predominantly expressed in Purkinje cells, completely lack long-term depression (LTD), a model of synaptic plasticity in the cerebellum. Moreover, a specific antibody against InsP3R1, introduced into wild-type Purkinje cells through patch pipettes, blocked the induction of LTD. These data indicate that, in addition to Ca2+ influx through Ca2+ channels on the plasma membrane, Ca2+ release from InsP3R plays an essential role in the induction of LTD, suggesting a physiological importance for InsP3R in Purkinje cells.
    Journal of Neuroscience 08/1998; 18(14):5366-73. · 6.91 Impact Factor
  • Neuroscience Research 01/1998; 31. · 2.20 Impact Factor

Publication Stats

897 Citations
143.11 Total Impact Points

Institutions

  • 2007
    • Kochi University
      • Department of Neuropsychiatry
      Kôti, Kōchi, Japan
  • 2003
    • Kochi Medical School
      Kôti, Kōchi, Japan
  • 1998–2001
    • The University of Tokyo
      • Institute of Medical Science
      Tokyo, Tokyo-to, Japan
    • Japan Science and Technology Agency (JST)
      Edo, Tōkyō, Japan
  • 2000
    • University of California, San Diego
      San Diego, California, United States
    • Nagoya City University
      • Department of Cell Physiology
      Nagoya, Aichi, Japan