Preliminary evidence for timing abnormalities in the CNTNAP2 knockout rat

The CNTNAP2 gene has been implicated in several neuropsychological disorders, including autism spectrum disorder (ASD) and schizophrenia. The CNTNAP2 knockout (KO) rat model, rats without the CNTNAP2 gene, exhibits deficits in social interaction and increases in both repetitive and anxiety-like behaviors. However, deficits in time perception that may underlie several of the neuropsychological disorders implicated have not been investigated. The current study investigated timing in CNTNAP2 KO rats compared to control rats using a discrete-trial temporal bisection task. Results suggested deficits in the timing of relatively long durations in the CNTNAP2 KO rats. This finding is consistent with similar findings previously reported in humans diagnosed with ASD, and is promising for understanding the role that the CNTNAP2 gene may play in timing in certain neuropsychological disorders, and for developing targeted clinical therapies.

Automated summary

Deficits in timing of relatively long durations were found in CNTNAP2 knockout rats, similar to findings in individuals with ASD. This suggests a potential role of the CNTNAP2 gene in timing and implications for targeted therapeutic interventions.