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Published on: November 20, 2015
Maternal Copper Deficiency Impairs the Developmental Expression of Protein Kinase C α, β and γ Isoforms in Neonatal
W T Johnson1, A C Thomas1, A A Lozano1
1a United States Department of Agriculture , Agricultural Research Service, Grand Forks Human Nutrition Research Center , P.O. Box 9034, Grand Forks , ND 58202-9034 , USA.
Abstract:
Although brain development and neurological function are impaired in the offspring of rodents that consume copper-deficient diets during pregnancy and lactation, the underlying mechanisms for the impairment are not well understood. Because protein kinase C (PKC) has been implicated in regulating development of the central nervous system, the present study was conducted to determine if maternal copper intake during pregnancy and lactation influences the expression of PKC in the developing brains of neonatal rats. Dams were fed diets containing either 1 μg Cu/g (Cu1), 2 μg Cu/g (Cu2), or 6 μg Cu/g (Cu6) beginning three weeks before pregnancy and ending 21 days after parturition. The α, β, and γ isoforms of PKC increased in the cytosolic fraction of neonatal brain during the 21 days following parturition, but the rates of increase for PKCβ and γ were significantly reduced in neonates of dams consuming Cu1 and Cu2. In a second experiment, PKCβ content in the cytosolic fraction of the hypothalamus and PKCγ content in the cytosolic fraction of the cerebellum were significantly lowered in 21-day-old pups of dams consuming Cu1 and Cu2. These data indicate that maternal diets that are deficient in copper impair the expression of PKCβ, and γ in the developing brain of neonatal rats.

