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Heavy metals: effects on synaptic transmission.

G P Cooper, J B Suszkiw, R S Manalis

    Neurotoxicology
    |January 1, 1984
    PubMed
    Summary
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    Heavy metals like lead (Pb++) and cadmium (Cd++) inhibit acetylcholine release at nerve synapses by blocking calcium (Ca++) channels. Mercury (Hg++) has a more complex effect, initially increasing release before blocking it.

    Area of Science:

    • Neuroscience
    • Toxicology
    • Biochemistry

    Background:

    • Synaptic transmission relies on precise ion channel function.
    • Heavy metals are known neurotoxins with varied mechanisms.

    Purpose of the Study:

    • To investigate the acute effects of lead (Pb++), cadmium (Cd++), and mercury (Hg++) on synaptic transmission.
    • To elucidate the biochemical mechanisms underlying heavy metal neurotoxicity at the synapse.

    Main Methods:

    • Electrophysiological studies on frog sciatic nerve-sartorius muscle preparations.
    • Biochemical analysis of synaptosomes from rat brains.
    • Measurement of acetylcholine (ACh) release, endplate potentials (EPPs), and miniature endplate potentials (MEPPs).
    • Assessment of 45Ca++ influx into synaptosomes.

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    Main Results:

    • Pb++ and Cd++ competitively inhibit evoked acetylcholine release by blocking presynaptic Ca++ channels, with dissociation constants of ~1 µM and ~2.8 µM, respectively.
    • Pb++ increases spontaneous transmitter release (MEPP frequency), suggesting intracellular Ca++ dysregulation, while Cd++ does not.
    • Hg++ initially enhances evoked ACh release before causing a complete blockade, with a similar time course for MEPP frequency.
    • Pb++ and Cd++ competitively inhibit K+-stimulated 45Ca++ influx in rat brain synaptosomes with dissociation constants of ~1.1 µM and ~2.2 µM, respectively.

    Conclusions:

    • The neurotoxic effects of Pb++ and Cd++ on synaptic transmission are primarily due to the inhibition of voltage-gated Ca++ influx into presynaptic nerve terminals.
    • Cd++ and Pb++ act as competitive inhibitors of Ca++ channels, impacting neurotransmitter release.
    • Hg++ exhibits a unique biphasic effect on synaptic transmission, warranting further investigation into its mechanism.