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Related Experiment Videos

PKC isoforms were reduced by lead in the developing rat brain.

Shang-Zhi Xu1, Latoya Bullock, Chun-Juan Shan

  • 1Department of Biological Sciences, Alcorn State University, 1000 ASU Drive, P.O. Box 870, Alcorn State, MS 39096, USA.

International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience
|February 26, 2005
PubMed
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Lead exposure in developing rats significantly reduced protein kinase C (PKC) isoforms and activity in the brain, particularly during early postnatal development. These effects were most pronounced in the hippocampus and frontal cortex.

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • Protein kinase C (PKC) isoforms are crucial for synaptic plasticity and neurotransmitter release.
  • The precise mechanisms of lead (Pb)-induced neurotoxicity involving PKC isoforms remain unclear.
  • PKC signaling pathways are implicated in various neuronal functions and developmental processes.

Purpose of the Study:

  • To investigate the impact of developmental lead exposure on various protein kinase C (PKC) isoforms in different regions of the developing rat brain.
  • To elucidate the temporal and regional effects of lead on PKC protein levels and enzymatic activity.
  • To understand the potential neurotoxic mechanisms of lead exposure during critical developmental windows.

Main Methods:

  • Sprague-Dawley rats were exposed to lead acetate from gestation through postnatal day 21.

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  • Brain regions including the brain stem, cerebellum, hippocampus, and frontal cortex were analyzed at different postnatal days (1, 5, 10, 45).
  • Lead levels, PKC isoform protein expression (Western blotting), and total PKC activity were quantified.

    • Main Results:

    • Lead exposure significantly reduced PKC isoform proteins (alpha, beta, gamma, epsilon, mu) in the hippocampus and frontal cortex, especially on postnatal day 5.
    • Reductions in PKC proteins were more pronounced in membrane fractions compared to cytosolic fractions.
    • Total PKC activity was inhibited by 70% on postnatal days 1 and 5, primarily affecting calcium-dependent activity.

    Conclusions:

    • Developmental lead exposure profoundly disrupts PKC signaling in the rat brain.
    • Early-life lead exposure leads to decreased PKC activity and reduced expression of key PKC isoforms, potentially impairing synaptic plasticity and cognitive functions.
    • The observed alterations in PKC isoforms, particularly PKC-gamma and epsilon, may underlie lead's detrimental effects on memory formation and long-term potentiation.