Synaptic up-and down-regulation by changes in intracellular calcium concentrations

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Glutamate is the major excitatory neurotransmitter in the cerebral cortex. After blockade of NMDA and non-NMDA ionotropic glutamate receptors, tetanization to presynaptic fibers were induced long-term depression. Further experiments with agonists and antagonists suggested that some G protein-linked, inositol-1,4,5-trisphosphate (IP3)-coupled types of metabotropic glutamate receptors (mGluRs) are involved in induction of this long-term depression. Intracellular injection of the G-protein inhibitor GDPbetaS or the IP3 receptor inhibitor heparin prevented long-term depression but allowed long-term potentiation induction. Also Ca^<2+> chelation by EGTA prevented long-term depression. These experiments suggest that Ca^<2+> released from cytosolic stores resulted in long-term depression, whereas Ca^<2+> influxes lead to long-term potentiation. It thus seems that Ca^<2+> source may determine the whole fate of synaptic regulation.