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; Pei et al., 1999; Mazarati et al., 2006), Parkinson’s disease and ataxia (Patil et al., 1995; Slesinger et al., 1996; Schein et al., 2005) and Down’s syndrome (Siarey et al., 1999; Cramer et al., 2010; Cooper et al., 2012). GIRK channels are implicated in motor activity, anxiety, reward and movement disorder (ataxia) (Pravetoni and Wickman, 2008). Recent studies have suggested possible role of KCNJ6/GIRK2 in bipolar disorder (Hamshere et al., 2009) and depression (Lazary et al., 2011). Further, there is also evidence to show that GIRK2/KCNJ6 function directly influences neuroelectric activity (EEG). For example, there are animal studies showing relationship between KCNJ6 and neuroelectric/seizure activity of the brain. A knockout mouse model found that animals deprived of functional KCNJ6 protein were susceptible to spontaneous and provoked seizures (cf. Hallmann et al., 2000). A recent study with a mouse model of seizure activity reported that GIRK2 channel (KCNJ6) may play a major role in the genesis of childhood epilepsy (infantile spasms)
