Relationship between prostaglandin synthesis and release of acidic amino acid neurotransmitters

The importance of glutamate as an excitatory neurotransmitter in the central nervous system has become increasingly clear. However, the presynaptic mechanism of amino acid neurotransmitter release does not appear to be consistent with existing models. A major source of controversy has been the finding that a significant amount of the amino acid release evoked by membrane depolarization is calcium-independent. It is often implied that this component of release is of cytosolic origin and subserves no neurotransmitter function. In this report, an alternative model is presented which suggests that the depolarization-induced movement of calcium ions into the nerve terminal acts, simultaneously, to stimulate the release of acidic amino acid neurotransmitters from both a vesicular and cytosolic compartment. According to this model, the influx of calcium may indirectly stimulate the biosynthesis of prostaglandins which lower the plasma membrane potential and reverse the electrogenic transport of amino acids to cause a net efflux. Such a mechanism could explain how the vesicular and cytosolic neurotransmitter pools of release are functionally related.