KCNJ6 gene encodes G-protein-coupled inwardly rectifying potassium channel 2 (GIRK2) which is one of four primary neuronal GIRK subunits, GIRK1-GIRK4 (Luscher and Slesinger, 2010). GIRK channels allow potassium ions to flow into the cell rather than out of the cell, a property referred to as “inward rectification” (Bodhinathan and Slesinger, 2014). GIRK channels have been shown to be critical for excitatory synaptic plasticity that underlies learning and memory, as GIRK2 null mutation or GIRK channel blockade has been found to abolish depotentiation of long-term potentiation in cultured hippocampal neurons (Chung et al., 2009). GIRK2 is also associated with opioid transmission in the brain and analgesic properties (Nishizawa et al., 2009). Further, GIRK2 is widely expressed in cerebellum, and an elevated expression of these channels may be involved in neuropathology, and contribute to a range of mental and functional disabilities in Down syndrome (Thiery et al., 2003; Harashima et al., 2006; Cramer et al., 2010). Alterations in GIRK channel function have been associated with pathophysiology of severe neurological disorders (cf. Bodhinathan and Slesinger, 2014), such as epilepsy (Signorini et al., 1997;
