[3H]Rolipram binding and phosphodiesterase activity in neuroblastoma N18TG-2 and glioma C6Bu-1

Tohda, Michihisa; Murayama, Toshihiko; Hasegawa, Hiroyuki; Nogiri, Shinsuke; Nomura, Yasuyuki

doi:10.1016/0304-3940(94)91085-5

Cited by 5 publications

(1 citation statement)

References 11 publications

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“…Gly, glycine, TPA, 12 0 tetradecanoylphorbol 13 acetate, QA: quiscalic acid, KA: kainic acid. [30][31][32][33][34][35][36][37][38][39] がん遺伝子 v Ki ras を導入し Cerebral stresses (ischemia and cytokines etc.) cause iNOS, chemokines and molecular chaperons which aŠect neuronal survival/death, brain edema and in-‰ammation.…”

Section: Fig 3 5 Ht Induced Cgmp Formation In Ng108 15 Cellsmentioning

confidence: 99%

Cellular and Molecular Pharmacological Studies on Membrane Receptor-Signaling and Stress-Responses in the Brain

Nomura

2001

YAKUGAKU ZASSHI

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Studies on the cellular and molecular mechanism of neurotransmitter receptor-signaling and of neuronal and glial cell responses to stresses seem to be important to elucidate the action mechanism of centrally-acting drugs and to develop novel therapeutics against several diseases in the brain. The present review shows ourˆndings with regard to the membrane receptor-signaling mechanism including serotonin, noradrenaline, glutamate receptors, ion channels, G proteins, protein kinases and drug actions in Xenopus oocytes injected with rat brain mRNA, NG108 15 cells and brain membranes. Regarding the results of studies on the inter-and intra-cellular mechanism of neurons and glial cells against cerebral ischemia/hypoxia, we review the involvement of a transcription factor NF kB in LPS elicited inducible NO synthase (iNOS) expression in rat astroglial cells. Then we describe possible involvement of: 1) ADP ribosylation/ nitrosylation of glyceraldehyde 3 phosphate dehydrogenase (GAPDH) and 2) decrease in mitochondrial membrane potential, release of caspase 3 from mitochondria and degradation of the inhibitor of caspase-activated DNase by activated caspase in NO-induced neuronal apoptosis. We observed that hypoxia results in expression of a molecular chaperon such as protein disulˆde isomerase (PDI) and HSP70 in astroglial cells. Our recentˆndings indicate that overexpression of PDI in the rat hippocampus (in vivo) and in neuroblastoma SK N MC cells (in vitro) signiˆcantly suppress the hypoxia-induced neuronal death. From physiological/pathophysiological and pharmacological aspects, we review the importance of studies on the cellular and molecular mechanism of membrane receptor-signaling and of stress-responses in the brain to identify functional roles of neuro-glial-as well as neuro-neuronal interaction in the brain.

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