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Original article 73 Lack of association between the -sensitive cation channel 2 (ACCN2) gene and anxiety spectrum disorders John M. Better, Songbook An, Michael C. Neal, Edwin J.C.G. van den Word,

Since genetic studies indicate that the anxiety genes, DRD2 and CTNAP2, also encode ion channel subunits, we examined relationships between the rat and human ASIC1 subunits in the central nervous system, examining the hypothesis that anxiety, as a result of lack of association between the -sensitive cation channel 2 (ACCN2) gene and ASIC1, would contribute to fear conditioning. Methods: Fear conditioning was carried out using the Person Test (Person 1970), whereby rats are forced to press a lever (n = 8). A second group received a saline injection (Person) and one group received a 1-h incubation (Person + placebo, n = 8). At Person + incubation, rats experienced fear conditioning. Results: Incubation of rats with -acidophilus salt (3H-ACID) produced a 2-fold increase in fear conditioning, corresponding to a 2-fold increase in fear conditioning in rats receiving placebo. Conclusions: Fear conditioning induced by -acidophilus salt was not associated with association between the -sensitive cation channel 2 (ACCN2) gene and ASIC1. Keywords: acidophilus salt, ASIC, fear conditioning, rat, rat behavior, rat anxiety, fear conditioning Introduction Fear conditioning has been used extensively in animal research as a model of anxiety disorders (Bodkin et al. 2000; Johnson et al. 2001). Fear conditioning has been shown to be mediated by several ion channels including (1) the voltage-dependent calcium-dependent sodium (Na), magnesium (Mg), and calcining gene-related peptide (CORP) channels (Gibson & D'Silva 1995), (2) the voltage-dependent potassium (K) channels (Celesta 1995), which are highly expressed during the extinction of fear following aversive stimuli or social deprivation (Bodkin & Shake 1995; Sade & Janssen 1995), (3) the sodium (Na) channels (Celesta 1994a), which were shown to be a critical component of the fear conditioning system (Wang et al. 2001b) and (4) the Ca2+/calmodulin-dependent protein kinase II (Catkin) channel. These ion channels are important in the initiation and maintenance of the neuronal activity and in a variety of pathological states.

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