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C Tomioka

Publications and source records attributed to C Tomioka.

5 recordsLinked to original sources
PubMed1992

Absence of early destructive changes of cytoskeletal proteins after transient ischemia in the rat.

We examined the changes in immunoreactivity of microtubuli-associated protein (MAP) 2 in dendrites by immunohistochemical analysis following 20 min of cerebral ischemia in the rat. A decrease of immunoreactivity of MAP 2 in dendrites in the CA1 subfield of the hippocampus was observed on days 3 and 7 but not on day 1 after ischemia. Early destructive changes of this protein were not observed, a finding which was confirmed by polyacrylamide gel electrophoresis analysis. We elucidated one factor which indicated that destruction of the dendrites of CA1 pyramidal neurons would not take place any earlier than the destruction of the neurons themselves after ischemia in rats.

Animals↗
PubMed1992

Resistance of hippocampal CA-1 noradrenergic fibers to five minutes of transient cerebral ischemia in the gerbil.

We examined changes in the tyrosine hydroxylase (TH)-immunoreactive fibers following 5 min of cerebral ischemia in gerbils using an immunohistochemical method 1, 3 and 30 days after ischemia. Almost all CA-1 pyramidal neurons were lost 3 days after ischemia, whereas noradrenergic fibers were maintained 30 days after ischemia. The present study demonstrated that TH-immunoreactive fibers and cells were resistant to transient ischemia, and that there was no sprouting or hyperactivity in noradrenergic systems after ischemia.

Adrenergic Fibers↗
PubMed1991

Decrease of pre-synaptic noradrenergic fiber density in rat hippocampus after transient ischemia.

The selective loss of hippocampal CA-1 pyramidal neurons has been reported not to be accompanied by damage to presynaptic terminals in the stratum radiatum as shown by electron microscopic observations. However, we examined changes in the tyrosine hydroxylase (TH) immunoreactive fibers following transient ischemia in rats using an immunohistochemical method 1, 3, 7 and 30 days after ischemia. The present study indicates that ischemic neuronal injury spreads to pre-synaptic fibers after the disappearance of the post-synaptic CA-1 pyramidal neurons.

Adrenergic Fibers↗
PubMed1983

A possible role of protein kinase C in signal-induced lysosomal enzyme release.

In platelets, activation of protein kinase C and mobilization of Ca2+ were selectively induced by the addition of 1-oleoyl-2-acetyl-glycerol and a low concentration of A23187, respectively (Kaibuchi, K., Takai, Y., Sawamura, M., Hoshijima, M., Fujikura, T. and Nishizuka, Y. (1983) J. Biol. Chem. 258, 6701-6704). Using this procedure evidence was obtained suggesting that the protein phosphorylation and Ca2+ mobilization were both essential and synergistically effective to cause release of lysosomal acid hydrolases such as N-acetylglucosaminidase. A similar observation was made for the lysosomal enzyme release from rat neutrophils.

Animals↗