Yasushi Kishimoto


Affiliation: Tokushima Bunri Univ
Location: Sanuki, Japan


  1. request reprint
    Kishimoto Y, Nakazawa K, Tonegawa S, Kirino Y, Kano M. Hippocampal CA3 NMDA receptors are crucial for adaptive timing of trace eyeblink conditioned response. J Neurosci. 2006;26:1562-70 pubmed
    ..These results indicate that CA3-NR1 KO mice are unable to rapidly retrieve adaptive CR timing, suggesting that CA3 NRs play a crucial role in the memory of adaptive CR timing in trace conditioning. ..
  2. Kishimoto Y, Higashihara E, Fukuta A, Nagao A, Kirino Y. Early impairment in a water-finding test in a longitudinal study of the Tg2576 mouse model of Alzheimer's disease. Brain Res. 2013;1491:117-26 pubmed publisher
    ..We therefore propose that the water-finding test is a rapid and sensitive method that can be used to assess cognitive and/or behavioral deficits in mouse models of Alzheimer's disease. ..
  3. Miyata M, Kishimoto Y, Tanaka M, Hashimoto K, Hirashima N, Murata Y, et al. A role for myosin Va in cerebellar plasticity and motor learning: a possible mechanism underlying neurological disorder in myosin Va disease. J Neurosci. 2011;31:6067-78 pubmed publisher
    ..Interestingly, d-n mice had defects of motor coordination from young to adult ages, suggesting that the role of myosin Va in PC spines is not sufficient for motor coordination. ..
  4. Wada N, Kishimoto Y, Watanabe D, Kano M, Hirano T, Funabiki K, et al. Conditioned eyeblink learning is formed and stored without cerebellar granule cell transmission. Proc Natl Acad Sci U S A. 2007;104:16690-5 pubmed
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    Kishimoto Y, Kano M. Endogenous cannabinoid signaling through the CB1 receptor is essential for cerebellum-dependent discrete motor learning. J Neurosci. 2006;26:8829-37 pubmed
    ..These results indicate that endogenous cannabinoid signaling through CB1 is essential for cerebellum-dependent discrete motor learning, especially for its acquisition. ..
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    Kishimoto Y, Fujimichi R, Araishi K, Kawahara S, Kano M, Aiba A, et al. mGluR1 in cerebellar Purkinje cells is required for normal association of temporally contiguous stimuli in classical conditioning. Eur J Neurosci. 2002;16:2416-24 pubmed
    ..In contrast, mGluR1 in other cell types is required for associating discontiguous stimuli and long-term memory formation in nonspatial hippocampus-dependent learning. ..
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    Kishimoto Y, Kawahara S, Mori H, Mishina M, Kirino Y. Long-trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit epsilon 1. Eur J Neurosci. 2001;13:1221-7 pubmed
  8. Kishimoto Y, Oku I, Nishigawa A, Nishimoto A, Kirino Y. Impaired long-trace eyeblink conditioning in a Tg2576 mouse model of Alzheimer's disease. Neurosci Lett. 2012;506:155-9 pubmed publisher
    ..The long-trace eyeblink conditioning could be a potential tool for detecting early cognitive deficits in AD mouse model. ..
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    Kina S, Tezuka T, Kusakawa S, Kishimoto Y, Kakizawa S, Hashimoto K, et al. Involvement of protein-tyrosine phosphatase PTPMEG in motor learning and cerebellar long-term depression. Eur J Neurosci. 2007;26:2269-78 pubmed
    ..These results suggest that tyrosine dephosphorylation events regulated by PTPMEG are important for both motor learning and cerebellar synaptic plasticity. ..

Detail Information


  1. Kakizawa S, Kishimoto Y, Hashimoto K, Miyazaki T, Furutani K, Shimizu H, et al. Junctophilin-mediated channel crosstalk essential for cerebellar synaptic plasticity. EMBO J. 2007;26:1924-33 pubmed
    ..Therefore, JPs support the Ca(2+)-mediated communication between voltage-gated Ca(2+) channels, RyRs and SK channels, which modulates the excitability of PCs and is fundamental to cerebellar LTD and motor functions. ..
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    Kishimoto Y, Kawahara S, Fujimichi R, Mori H, Mishina M, Kirino Y. Impairment of eyeblink conditioning in GluRdelta2-mutant mice depends on the temporal overlap between conditioned and unconditioned stimuli. Eur J Neurosci. 2001;14:1515-21 pubmed
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    Kishimoto Y, Hirono M, Sugiyama T, Kawahara S, Nakao K, Kishio M, et al. Impaired delay but normal trace eyeblink conditioning in PLCbeta4 mutant mice. Neuroreport. 2001;12:2919-22 pubmed
    ..Rostral cerebellar LTD may be required as a neural substrate for delay conditioning, but is not required for trace conditioning. ..
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    Takatsuki K, Kawahara S, Takehara K, Kishimoto Y, Kirino Y. Effects of the noncompetitive NMDA receptor antagonist MK-801 on classical eyeblink conditioning in mice. Neuropharmacology. 2001;41:618-28 pubmed
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    Hirono M, Sugiyama T, Kishimoto Y, Sakai I, Miyazawa T, Kishio M, et al. Phospholipase Cbeta4 and protein kinase Calpha and/or protein kinase CbetaI are involved in the induction of long term depression in cerebellar Purkinje cells. J Biol Chem. 2001;276:45236-42 pubmed
    ..Taken together, these results suggest that mGluR1-mediated activation of PLCbeta4 in rostral cerebellar Purkinje cells induced LTD via PKCalpha and/or PKCbetaI. ..
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    Kishimoto Y, Kawahara S, Kirino Y, Kadotani H, Nakamura Y, Ikeda M, et al. Conditioned eyeblink response is impaired in mutant mice lacking NMDA receptor subunit NR2A. Neuroreport. 1997;8:3717-21 pubmed
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    Kishimoto Y, Suzuki M, Kawahara S, Kirino Y. Age-dependent impairment of delay and trace eyeblink conditioning in mice. Neuroreport. 2001;12:3349-52 pubmed
    ..These results indicate that trace eyeblink conditioning is more susceptible to age-related deterioration of memory in mice than delay eyeblink conditioning. ..
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    Kishimoto Y, Kawahara S, Suzuki M, Mori H, Mishina M, Kirino Y. Classical eyeblink conditioning in glutamate receptor subunit delta 2 mutant mice is impaired in the delay paradigm but not in the trace paradigm. Eur J Neurosci. 2001;13:1249-53 pubmed
    ..Thus, the present study has revealed a cerebellar LTD-independent learning in eyeblink conditioning. ..
  9. Shishido H, Kishimoto Y, Kawai N, Toyota Y, Ueno M, Kubota T, et al. Traumatic brain injury accelerates amyloid-? deposition and impairs spatial learning in the triple-transgenic mouse model of Alzheimer's disease. Neurosci Lett. 2016;629:62-67 pubmed publisher
    ..The present study suggests that TBI could be a risk factor for accelerated AD progression, particularly when genetic and hereditary predispositions are involved. ..