0032 ADA Functional Polymorphism Modulates REM Sleep Following Total Sleep Deprivation

Abstract Introduction Adenosine Deaminase (ADA) regulates extracellular levels of adenosine, a brain correlate sleep homeostasis. A single nucleotide polymorphism (SNP) the ADA gene (rs73598374) is known to be associated with increased homeostatic pressure for NREM after total deprivation (TSD). Whether this genotype effect also impacts REM TSD has not been systematically investigated. The limit cycle reciprocal interaction model posits that NREM/REM cycles are regulated by cholinergic and GABAergic neurotransmitter systems. While regulation thought mediated state, evidence an association adenosine reported. Here we investigate influence on at baseline following TSD. Methods N=48 healthy, normal sleepers (ages 27.7 + 5.3, 23 females) participated in one three in-laboratory studies. Following 10h (22:00–08:00), participants underwent 38h TSD, subsequent recovery (22:00–08:00). Sleep periods were recorded polysomnographically scored visually according AASM criteria. Genomic DNA was extracted from whole blood, SNP assayed using real-time PCR. stages analyzed mixed-effect ANOVA fixed effects genotype, night (baseline vs. recovery), their interaction, controlling study, random over subject intercept. Results frequency genotypes (G/G: 42, A/G: 6) did vary Hardy-Weinberg equilibrium. There no time (p>0.7). However, allele carriers spent more during less compared G/G homozygotes (genotype interaction: F[1,46]=8.13, p=0.007). Conversely, while statistically significant (p>0.1), homozygotes. Conclusion shift balance between baseline, as well changes therein without concomitant time. This suggests role mediating regulation, possibly through REM. Support (if any) CDMRP W81XWH-05-1-0099; ONR N00014-13-C-0063; NIH R21CA16769; ARO W911NF2210223.