Corticostriatal and midbrain projections originate from several areas of the cerebral cortex and the midbrain [22], and release neurotransmitters including glutamate, dopamine and gamma-aminobutyric acid (GABA) into the dorsal striatum [23–25]. Both LTP and LTD have been found at corticostriatal synapses on medium-sized spiny neurons, in vitro and in vivo [26–28]. While LTD was reported to be the major form of corticostriatal plasticity, it has been reported that LTP and LTD can be induced by the high frequency stimulation (HFS) of corticostriatal fibers [29]. Notably, several factors have been implicated in modulating LTP and LTD at corticostriatal synapses. For example, in the presence of physiological concentration of magnesium, HFS can induce LTD in vitro [30]. Next, at low magnesium concentrations, HFS in the lateral striatum produces NMDA receptor (NMDAR)-dependent LTP as it is blocked by DL-2-amino-5-phosphonovaleric acid (AP-5), an NMDAR antagonist [29]. Furthermore, the anatomical location of the synapses within the dorsal striatum seems to influence the polarity of the observed corticostriatal plasticity. For instance, if the HFS is conducted in the dorsolateral striatum, which receives input primarily from sensorimotor
