| Abstrakt: |
At 4 h during pilocarpine-induced status epilepticus (DPISE) in rat, protein kinase C (PKC)β1, PKCβ2, and PKCγ were induced at the border between the stratum oriens and alveus (O/A border) of CA1 in the hippocampus. Induced PKCγ was colocalized with metabotropic glutamate receptor α (mGluRα). By intracerebroventricular injection of mGluR1α antagonists, (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), PKCβ1, PKCβ2, and PKCγ immunoreactive products decreased dramatically; however, intracerebroventricular injection of saline did not change the expression of PKCβ1, PKCβ2, and PKCγ, suggesting that these three PKC isoforms might be involved in mGluR1α-related excitoneurotoxicity. One day after pilocarpine-induced status epilepticus (APISE), PKCδ was induced in microglial cells. At this time point, both PKCγ and PKCε immunopositive products decreased in the inner molecular layer of upper blade of the stratum granulosum. At 731 days APISE, induced PKCβ1, PKCδ, PKCη, and PKCζ positive astrocytes were demonstrated in all parts of hippocampus, suggesting that they may be involved in gliosis. By this time, both PKCγ and PKCε immunopositive products in the inner molecular layer had almost disappeared, suggesting that they may be involved in the inhibition of granule cells by controlling neurotransmitter release presynaptically in the dentate gyrus of normal rats. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR] |
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