In the prelimbic cortex of the striatum, three forms or LTD have been established. The mechanism of the first is similar to CA1-LTD: a low frequency stimulus induces LTD by activation of NMDA receptors, with postsynaptic depolarization and increased postsynaptic calcium influx. The second is initiated by a high frequency stimulus and is arbitrated by presynaptic mGlu receptor 2 or 3, resulting in a long term reduction in the involvement of P/Q-type calcium channels in glutamate release. The third form of LTD requires endocannabinoids, activation of mGlu receptors and repetitive stimulation of glutamatergic fibers (13 Hz for ten minutes), resulting in a long-term decrease in presynaptic glutamate release. It is proposed that LTD in GABAergic striatal neurons leads to a long-term decrease in inhibitory effects on the basal ganglia, influencing the storage of motor skills.
