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Fumihiko Okada

Researcher at Hokkaido University

Publications -  49
Citations -  663

Fumihiko Okada is an academic researcher from Hokkaido University. The author has contributed to research in topics: Adenylate kinase & Cyclase. The author has an hindex of 13, co-authored 49 publications receiving 650 citations.

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G-proteins (Gi, Go) in the basal ganglia of control and schizophrenic brain

TL;DR: The level of Gi/Go was significantly decreased by 42% in the putamen of the left hemisphere in schizophrenics; caudate head and globus pallidus levels were unchanged.
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G proteins (Gi, Go) in the medial temporal lobe in schizophrenia: preliminary report of a neurochemical correlate of structural change.

TL;DR: This data is the first report of a neurochemical correlate of the structural change in the brains of patients with schizophrenia, and the amount of Gi or Go was reduced on the left side in the hippocampus, amygdala and parahippocampal gyrus.
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Pertussis toxin attenuates 5-hydroxytryptamine1A receptor-mediated inhibition of forskolin-stimulated adenylate cyclase activity in rat hippocampal membranes.

TL;DR: The data indicate that the inhibitory guanine nucleotide‐binding protein or Go (a similar GTP‐bindingprotein of unknown function purified from brain) mediates the 5‐HT1A agonist inhibition of hippocampal adenylate cyclase.
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Reduced concentrations of the α-subunit of GTP-binding protein Go in schizophrenic brain

TL;DR: There was a significant decrease in Goα in the hippocampus and caudate head of the right hemisphere in schizophrenic patients compared to controls; the ANOVA (a general linear model; SAS Type II) demonstrated a significant diagnosis × side interaction only in the amygdala.
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Possible involvement of pertussis toxin substrates (Gi, Go) in desipramine-induced refractoriness of adenylate cyclase in cerebral cortices of rats.

TL;DR: Coupling of β‐adrenergic receptors to adenylate cyclase in the brain membrane was impaired by the desipramine treatment, suggesting that the desensitization might be overcome when the inhibitory interaction of Gi on the subsequent process is attenuated by IAP treatment.