실험적 뇌허혈이 대뇌피질의 Protein Kinase C Isozyme발현에 미치는 영향 = Effects of Experimental Ischemia on Expression of Protein Kinase C Isozyme in Rat Neocortex

다국어 초록 (Multilingual Abstract)

Ischemia leads to a complex sequence of events culminating in the loss of functional integrity of the nervous system and, ultimately, in neuronal cell death. Intracellular accumulation of calcium ions following ischemia may alter protein kinase C(PKC) activity. But nature of change of the PKC activity depending on duration and degree of ischemia is not well understood.
To understand the effect of the experimental focal ischemia on expression of PKC isozyme, we investigated the expression of PKC y, fl, a immunocytochemically and activities of cytoch-rome oxidase(C0) histochemically in focal ischemic brain of the rat. Two groups of focal ischemic infarction were produced in two groups of Sprague Dawley rats(200-3oOgm) : Group Ⅰ, Clip compression of left middle cerebral artery (MCA) for lomin and release and sacrificed 48hr later : Group Ⅱ, Electric coagulation of left MCA and killed 2-24hr later.
In the group Ⅰ, CO activity and immunoreactivity(1R) for PKC y and B were decreased generally in the left MCA territory, especially in layers Ⅱ through Ⅳ of ischemic cortex In the group Ⅱ, decrease of CO activities and marked increase of three PKC isozyme 1% were noted in the layers I through Ⅵ. The isozymes displayed different localization in the control cortex, but the IRs of three isozymes markedly increased in the ischemic region, so that the difference among IR patterns disappeared Although vacuolation and decrease of number of IR neuron were noted, there were remaining IR pyramidal neurons around vacuole in layers IV/V showing dense immuostaining in the cell body and apical dendrite.
These results indicate that lomin acute ischemia inhibits activity of PKC y and i3 and that prolonged ischemia longer than 2hr induces the expression of three PKC isozymes. Inhibition and possible induction of PKC are proposed to represent a critical step during ischemic neuronal injury.