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Calcium‐Dependent Evoked Release of N [ 3 H]Acetylaspartylglutamate from the Optic Pathway
Author(s) -
Tsai Guochuan,
Forloni Gianluigi,
Robinson Michael B.,
Stauch Barbara L.,
Coyle Joseph T.
Publication year - 1988
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.1471-4159.1988.tb01186.x
Subject(s) - veratridine , depolarization , glutamate receptor , optic tract , superior colliculus , neuropeptide , neurotransmitter , biophysics , tetrodotoxin , chemistry , biochemistry , neuroscience , biology , central nervous system , optic nerve , receptor , sodium channel , sodium , organic chemistry
N ‐Acetylaspartylglutamate (NAAG) is a neuropeptide localized to several putative glutamatergic neuronal systems, including the rodent optic pathway. To determine whether the peptide is released by depolarization, the superior colliculus of the rat was perfused with 2 μCi of [ 3 H]NAAG, then with Krebs‐bicarbonate buffer for 1 h, using a microdialysis system. Subsequently, 10‐min fractions were collected and analyzed by HPLC for [ 3 H]NAAG. Addition of 100 μ M veratridine resulted in a several‐fold increase in the evoked release of [ 3 H]NAAG that was virtually abolished by coperfusion with Ca 2+ ‐free Krebs buffer containing 1 m M EGTA. When [ 3 H]glutamate was used as the precursor, veratridine depolarization resulted in only an 80% increase in the release of [ 3 H]NAAG. Prior enucleation of the right eye reduced the spontaneous release of [ 3 H]NAAG by 50%, and the veratridine‐evoked release by greater than 85%, from the left superior colliculus. These results suggest that NAAG is released upon depolarization and may serve as a neurotransmitter/neuromodulator in the optic tract.