Abstract
The role of glutamate transporters in the regulation of synaptic depression was examined in the avian nucleus magnocellularis. Repetitive stimulation of presynaptic auditory nerve fibers resulted in acute depression of EPSCs. Pharmacological blockade of glutamate transport in glial cells enhanced residual glutamate in the synaptic cleft and markedly increased the extent of depression at stimulus frequencies above 20 Hz via a postsynaptic mechanism. Glutamate pyruvate transaminase, a glutamate scavenger, accelerated the decay of the EPSC and reduced synaptic depression, indicating that transporters are not completely effective in rapid removal of glutamate. Regulation of residual transmitter by glia may thus serve to control synaptic strength in a frequency-dependent manner.