NDLI: Protein Kinase C in Rat Brain Is Altered by Developmental Lead Exposure

Content Provider	Springer Nature Link
Author	Chen, Hwei Hsien Ma, Tangeng Ho, Ing K.
Copyright Year	1999
Abstract	The absence of learning-related redistribution of hippocampal protein kinase C (PKC) has been correlated with impairment of learning performance induced by developmental lead (Pb) exposure. This study was designed to examine whether the properties of brain PKC are altered by chronic Pb exposure during development. Two-tenth percent Pb acetate was administered to pregnant and lactating dams and then administered to weanlings in drinking water until postnatal day (PN) 56. Effects of Pb on translocation of PKC were studied in brain slices prepared from hippocampus. When the slices were treated with 0.33 μM phorbol-12, 13-dibutyrate (PDBu) for 15 min, a significant increase in PKC activity was observed in the membrane fraction of hippocampal slices from Pb-exposed rats, suggesting that chronic Pb exposure potentiates PDBu-activated PKC translocation. Data obtained from saturation binding assays in the frontal cortices of Pb-exposed rats showed a decrease in the dissociation constant (K$_{D}$) in both membrane and cytosolic PKC. A decrease in the total binding sites (B$_{max}$) of [$^{3}$H]PDBu binding was only observed in membrane PKC. Furthermore, developmental Pb exposure decreased PKC-γ, but not PKC-α, -βII, and -ε in the membrane fraction of the hippocampus and the frontal cortex. These results indicate that chronic Pb exposure during development increases phorbol ester binding affinity, enhances phorbol ester-induced translocation of PKC, and down-regulates membrane PKC, mainly PKC-γ.
Starting Page	415
Ending Page	421
Page Count	7
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	24
Issue Number	3
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1999-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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