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α‐Latrotoxin Releases Both Vesicular and Cytoplasmic Glutamate from Isolated Nerve Terminals
Author(s) -
McMahon Harvey T.,
Rosenthal Luann,
Meldolesi Jacopo,
Nicholls David G.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb05793.x
Subject(s) - glutamate receptor , cytoplasm , synaptosome , amino acid , biology , biochemistry , biophysics , liberation , glutamic acid , synaptic vesicle , vesicle , membrane , in vitro , receptor
α‐Latrotoxin causes a massive release of endogenous glutamate from guinea‐pig cerebrocortical synaptosomes. There appear to be two components to the release. In the first 2 min following addition of 1.3 n M α‐latrotoxin, glutamate release is largely energy dependent. Superimposed upon this release is a more slowly developing but ultimately much more extensive release of cytoplasmic glutamate together with γ‐aminobutyric acid and nonvesicular amino acids such as aspartate and α‐aminoisobutyrate. In parallel with this cytoplasmic release there is an extensive depletion of ATP, a massive rise in cytoplasmic free Ca 2+ concentration, and a severe restriction of synaptosomal respiratory capacity. The cytoplasmic release is only partially Na + dependent. eliminating a simple reversal of the plasma membrane acidic amino acid carrier. It is concluded that α‐latrotoxin releases both transmitter and cytoplasmic pools of amino acids in synaptosomes and causes a major disruption of terminal integrity.