1. We have examined plasticity at glutamatergic synapses on neurons in
slices of neostriatum, a forebrain area involved in movement and cogn
itive function. 2. High-frequency stimulation of afferent inputs to ne
ostriatal neurons induced depression of glutamatergic synaptic transmi
ssion. Depression could be induced using either prolonged trains or sh
ort repetitive bursts of high-frequency stimulation. Depression develo
ped within seconds after such stimulation. Responses recovered to base
line levels within 10 min in most slices but persisted for up to 60 mi
n in others. 3. Postsynaptic passive electrical properties and the abi
lity to elicit action potentials by postsynaptic depolarization were n
ot altered during depression.4. The magnitude and time course of depre
ssion was similar whether postsynaptic responses were mediated by alph
a amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) or N-meth
yl-D-aspartate (NMDA) type glutamate receptors. Depression was not alt
ered by antagonism of AMPA or NMDA receptors or potentiation of AMPA r
eceptor function with aniracetam. 5. Depression was blocked by treatme
nts that increase transmitter release including increased extracellula
r Ca2+, application of 4-aminopyridine, or application of phorbol este
r. 6. Our findings indicate that glutamatergic synapses in neostriatum
are capable of expressing a form of synaptic depression that may invo
lve decreased glutamate release.