Abstract
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.
Highlights
Sensorimotor gating is the ability of a sensory stimulus to suppress a motor response[1]
Pten mutant mice are another model of autism and can be used to investigate the connection between a cell signaling pathway commonly implicated in autism spectrum disorder (ASD), the PI3K/AKT/mTOR pathway, and specific autistic-like deficits[8]
When assessing the sensorimotor gating paradigm, no main effects were found for habituation (F[1,27] = 0.17, p >0.05), prepulse inhibition (F[1,23] = 2.65, p >0.05) or startle threshold (F[1,16] = 2.33, p >0.05)
Summary
Sensorimotor gating is the ability of a sensory stimulus to suppress a motor response[1]. Pten mutant mice are another model of autism and can be used to investigate the connection between a cell signaling pathway commonly implicated in ASD, the PI3K/AKT/mTOR pathway, and specific autistic-like deficits[8]. We use neuronal subset-specific (NS)-Pten KO mice that exhibit hyperactivation of the PI3K/AKT/mTOR pathway in the cortex, hippocampus, and cerebellum, and assess PPI in order to further elucidate the potential relationship between PI3K/AKT/ mTOR signaling and deficits in sensorimotor gating[9]. It would be helpful if the neuronal subset-specific Pten KO mouse was described in more detail. The present findings help to elucidate the relationship between PI3K/AKT/mTOR hyperactivation and sensory reactivity
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
