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 cortex, the major form of plasticity is LTD. However, if HFS is conducted in the dorsomedial striatum, the major form of plasticity is LTP [26, 31–33]. The mechanisms underlying this distinct and varied effect in the striatal sub-regions is currently unknown, but could be due to the differential expression patterns of dopamine D2-like receptors [34]. Perhaps, reduced expression of D2-like receptors in dorsomedial striatum could favor the induction of LTP vs. LTD. Nevertheless, the presence or absence of magnesium and the anatomical location are not the only factors influencing the induction of LTP and LTD. Additional cellular mechanisms underlying the regional difference in the form of plasticity in the dorsal striatum include differences in presynaptic release in neurotransmitters, such as GABA vs. glutamate or dopamine. Indeed LTP is increased medially with HFS, and the effect is dependent on the blockade of GABAA receptors, as well as the elimination of dopaminergic input from nigrostriatal synapses [35]. Next, the age of the
