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  • Title: L-aspartate as an amino acid neurotransmitter: mechanisms of the depolarization-induced release from cerebrocortical synaptosomes.
    Author: Cavallero A, Marte A, Fedele E.
    Journal: J Neurochem; 2009 Aug; 110(3):924-34. PubMed ID: 19549007.
    Abstract:
    The role of L-aspartate as a classical neurotransmitter of the CNS has been a matter of great debate. In this study, we have characterized the main mechanisms of its depolarization-induced release from rat purified cerebrocortical synaptosomes in superfusion and compared them with those of the well known excitatory neurotransmitter L-glutamate. High KCl and 4-aminopyridine were used as depolarizing agents. At 15 mM KCl, the overflows of both transmitters were almost completely dependent on external Ca2+. At 35 and 50 mM KCl, the overflows of L-aspartate, but not those of L-glutamate, became sensitive to DL-threo-b-benzyloxy aspartic acid (DL-TBOA), an excitatory amino acid transporter inhibitor. In the presence of DL-TBOA, the 50 mM KCl-evoked release of L-aspartate was still largely external Ca2+-dependent. The DL-TBOA insensitive,external Ca2+-independent component of the 50 mM KCl-evoked overflows of L-aspartate and L-glutamate was significantly decreased by the mitochondrial Na+/Ca2+ exchanger blocker CGP 37157. The Ca2+-dependent, KCl-evoked overflows of L-aspartate and L-glutamate were diminished by botulinum neurotoxin C, although to a significantly different extent. The 4-aminopyridine-induced L-aspartate and L-glutamate release was completely external Ca2+-dependent and never affected by DL-TBOA. Superimposable results have been obtained by pre-labeling synaptosomes with [3H]D aspartate and [3H]L-glutamate. Therefore, our data showing that L-aspartate is released from nerve terminals by calcium dependent,exocytotic mechanisms support the neurotransmitter role of this amino acid.
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