Neuronal subset-specific Pten-deficient mice do not exhibit deficits in sensorimotor gating processes

Background: Deficits in sensorimotor gating have been reported in individuals with autism spectrum disorder (ASD), as well as in ASD murine models. However, this behavior has been rarely examined in the neuronal subset-specific (NS)- Pten  knockout (KO) model of ASD. NS-Pten KO mice exhibit hyperactivity of the PI3K/AKT/mTOR signaling pathway which is implicated in the onset of autistic deficits. This study investigates the potential relationship between PI3K/AKT/mTOR signaling and deficits in sensorimotor gating.    Methods: To assess sensorimotor gating in NS- Pten  KO mice we utilized a three-day paradigm. On day 1 (habituation) the mice were administered 80 repetitions of a 120-dB startle stimulus. On day 2, prepulse inhibition was measured with 90 trials of the startle stimulus that was paired with a smaller (70, 75, or 80 dB) prepulse stimulus. Day 3 was assessed one week later, consisting of randomized startle trials and trials with no stimulus and was used to determine the startle threshold. Results: No significant difference between NS- Pten  KO or wildtype (WT) mice was found for habituation ( p > 0.05). No significant differences were found between groups when assessing the percentage of prepulse inhibition at 70, 75, and 80 dB ( p > 0.05). There was also no difference in startle threshold between groups ( p > 0.05). Conclusion: Our study found that the NS- Pten  KO model does not display significant deficits in sensorimotor gating processes. The present findings help to elucidate the relationship between PI3K/AKT/mTOR hyperactivation and sensory reactivity.