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[Latrotoxin channels. Permeability for divalent cations].

V K Lishko, E A Saĭchenko, L G Storchak

    Biokhimiia (Moscow, Russia)
    |September 1, 1990
    PubMed
    Summary
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    Alpha-latrotoxin forms channels that transport calcium ions (Ca2+) into synaptosomes, following Michaelis-Menten kinetics. Other divalent cations also use these channels, impacting synaptosome membrane potential.

    Area of Science:

    • Neuroscience
    • Biophysics
    • Molecular Biology

    Context:

    • Synaptosomes are crucial for neurotransmission, and their function is highly dependent on calcium ion (Ca2+) regulation.
    • Alpha-latrotoxin (LTX) is a potent neurotoxin that induces massive neurotransmitter release by forming cation-selective channels in presynaptic terminals.
    • Understanding the properties of LTX-induced channels is vital for elucidating calcium signaling pathways and neuronal excitability.

    Purpose:

    • To investigate the quantitative characteristics of Ca2+ transport through LTX channels in synaptosomes.
    • To determine the feasibility of other divalent cations traversing LTX channels.
    • To explore the functional consequences of cation influx on synaptosome membrane potential.

    Summary:

    • Calcium influx into synaptosomes via alpha-latrotoxin channels exhibits nonlinear dependence on intracellular calcium concentration, adhering to Michaelis-Menten kinetics with a Km of 1.07 ± 0.19 mM.

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  • Divalent cations including Mg2+, Ba2+, Sr2+, Mn2+, and Co2+ were found to competitively inhibit Ca2+ influx and also permeate the LTX channels, as confirmed by fluorescent probes Quin-2 and Fura-2.
  • The influx of these divalent cations through LTX channels leads to a decrease in synaptosome membrane potential, suggesting a role in modulating neuronal excitability.

    • Impact:

    • This study provides quantitative insights into the ion transport properties of alpha-latrotoxin channels.
    • The findings suggest potential similarities between LTX channels and endogenous calcium channels, offering a model for studying calcium homeostasis.
    • Understanding these mechanisms can contribute to developing strategies for modulating neuronal activity in neurological disorders.