SLC9A9 is ubiquitously expressed and may play a role in basic cellular functioning (Nakamura et al., 2005). There is evidence suggesting that SLC9A9 interacts with RACK1, which is a scaffolding protein found in the brain (Ohgaki et al., 2008). In addition, a recent study showed that SLC9A9 was significantly upregulated as a result of the RNAi knock-down of NPAS4, which is a transcription factor that is activated in response to neuronal membrane depolarization (Morrow et al., 2008). Although SLC9A9 expression was unaltered in response to neuronal membrane depolarization alone (Morrow et al., 2008), it seems to be either directly or indirectly regulated by a transcription factor induced by neuronal activity. Furthermore, several functional studies showed that SLC9A1 (member of the SLC9A family) null mice have increased hippocampal neuronal excitability, signs of ataxia, and seizures (Cox et al., 1997; Bell et al., 1999; Gu et al., 2001). Interestingly, seizure-prone rat strains exhibit common characteristics of AD/HD and autism spectrum disorders (Gilby, 2008).
