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Two Components of Glutamate Exocytosis Differentially Affected by Presynaptic Modulation
Author(s) -
Herrero I.,
Castro E.,
MirasPortugal M. T.,
SánchezPrieto J.
Publication year - 1996
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 - 10.1046/j.1471-4159.1996.67062346.x
Subject(s) - glutamate receptor , biophysics , chemistry , exocytosis , metabotropic glutamate receptor , depolarization , agonist , glutamic acid , adenosine , neurotoxin , metabotropic receptor , metabotropic glutamate receptor 2 , biochemistry , receptor , biology , amino acid , membrane
The total Ca 2+ ‐dependent release of glutamate induced by depolarization of cerebrocortical nerve terminals with KCl was analyzed into a fast and a slow component. The fast component exhibited a decay time of <1 s and accounted for 0.95 ± 0.10 nmol of glutamate, whereas the slow component, which exhibited a decay time of 52 ± 7 s, accounted for the release of 2.48 ± 0.19 nmol of glutamate. These two components were differentially affected by the Ca 2+ chelator BAPTA, the divalent cation Sr 2+ , or the botulinum neurotoxin A. The adenosine A 1 receptor agonist N 6 ‐cyclohexyladenosine strongly reduced the fast component without altering the slow component. In contrast, the inhibitory effect of arachidonic acid and the facilitatory action of the metabotropic glutamate receptor agonist (1 S ,3 R )‐1‐aminocyclopentane‐1,3‐dicarboxylic acid were observed as a decrease and an increase, respectively, in the two components. It is concluded, first, that the fast and slow components correspond to the release of docked and mobilized vesicles, respectively, and second, that presynaptic modulation more significantly alters the fast component of release.