about
Genetic neuroscience of mammalian learning and memoryGABAergic interneuron origin of schizophrenia pathophysiology.Hippocampal CA3 NMDA receptors are crucial for memory acquisition of one-time experienceCA3 NMDA receptors are crucial for rapid and automatic representation of context memoryEssential function of alpha-calcium/calmodulin-dependent protein kinase II in neurotransmitter release at a glutamatergic central synapse.Requirement for hippocampal CA3 NMDA receptors in associative memory recallSpatial and temporal boundaries of NMDA receptor hypofunction leading to schizophrenia.Dysregulation of the axonal trafficking of nuclear-encoded mitochondrial mRNA alters neuronal mitochondrial activity and mouse behaviorBrain state-dependent abnormal LFP activity in the auditory cortex of a schizophrenia mouse model.Social isolation exacerbates schizophrenia-like phenotypes via oxidative stress in cortical interneuronsContribution of NMDA receptor hypofunction in prefrontal and cortical excitatory neurons to schizophrenia-like phenotypes.Lack of kainic acid-induced gamma oscillations predicts subsequent CA1 excitotoxic cell death.eIF2alpha Phosphorylation-dependent translation in CA1 pyramidal cells impairs hippocampal memory consolidation without affecting general translation.Loss of GluN2B-containing NMDA receptors in CA1 hippocampus and cortex impairs long-term depression, reduces dendritic spine density, and disrupts learning.GluN2B in corticostriatal circuits governs choice learning and choice shifting.Preferential inactivation of Scn1a in parvalbumin interneurons increases seizure susceptibilityPostnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes.Chronic stress-induced hippocampal dendritic retraction requires CA3 NMDA receptorsNMDA receptor subunits and associated signaling molecules mediating antidepressant-related effects of NMDA-GluN2B antagonism.Impaired discrimination learning in interneuronal NMDAR-GluN2B mutant miceInducible and cell-type restricted manipulation in the entorhinal cortex.Hilar mossy cell degeneration causes transient dentate granule cell hyperexcitability and impaired pattern separation.Hilar mossy cell circuitry controlling dentate granule cell excitability.Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia.Identification of transcription factors for lineage-specific ESC differentiation.Cortical GluN2B deletion attenuates punished suppression of food reward-seeking.NMDA receptor-dependent ocular dominance plasticity in adult visual cortex.Notch1 signaling in pyramidal neurons regulates synaptic connectivity and experience-dependent modifications of acuity in the visual cortex.Hippocampal CA3 NMDA receptors are crucial for adaptive timing of trace eyeblink conditioned response.Schizophrenia-Like Dopamine Release Abnormalities in a Mouse Model of NMDA Receptor Hypofunction.Neuropsychiatric Phenotypes Produced by GABA Reduction in Mouse Cortex and Hippocampus.Transient and persistent phosphorylation of AMPA-type glutamate receptor subunits in cerebellar Purkinje cells.AMPA Receptor Activation-Independent Antidepressant Actions of Ketamine Metabolite (S)-NorketamineAntibody specific for phosphorylated AMPA-type glutamate receptors at GluR2 Ser-696Immunohistochemical localization of protein phosphatase isoforms in the rat cerebellumThe origin of NMDA receptor hypofunction in schizophrenia
P50
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P50
description
hulumtues
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Kazutoshi Nakazawa
@ast
Kazutoshi Nakazawa
@en
Kazutoshi Nakazawa
@es
Kazutoshi Nakazawa
@nl
Kazutoshi Nakazawa
@sl
type
label
Kazutoshi Nakazawa
@ast
Kazutoshi Nakazawa
@en
Kazutoshi Nakazawa
@es
Kazutoshi Nakazawa
@nl
Kazutoshi Nakazawa
@sl
prefLabel
Kazutoshi Nakazawa
@ast
Kazutoshi Nakazawa
@en
Kazutoshi Nakazawa
@es
Kazutoshi Nakazawa
@nl
Kazutoshi Nakazawa
@sl
P1153
P1053
J-6195-2015
P106
P1153
56099045300
7202920816
7202920906
P21
P31
P3829
P3835
kazutoshi-nakazawa
P496
0000-0001-5699-9093