This study addresses the critical need to improve understanding and treatment options for individuals suffering from obsessive-compulsive disorder (OCD), for which we have limited therapeutic interventions. By investigating the genetic association between the SLC1A1 gene and OCD in humans and exploring its impact in rodent models, this research narrows the translational gap, offering insights into the neurobiological mechanisms underlying OCD-relevant behaviors.
The development of a new mouse model with reversible overexpression of Slc1a1 in the forebrain represents a significant advance in the field, allowing researchers to manipulate gene expression and investigate its effects on behavior, particularly in response to amphetamine, a substance known to exacerbate symptoms. of OCD. Importantly, through the use of an unbiased machine learning classifier, this study identified different patterns of amphetamine-induced behaviors in mice with Slc1a1 overexpression, elucidating the complex relationship between genetic predisposition and environmental triggers in the manifestation of OCD-like behaviors. .
Finally, the observed increase in neuronal activation in the ventromedial striatum (among other areas) highlights potential targets for future therapeutic interventions based on neuromodulation, aiming to attenuate repetitive behaviors associated with OCD, paving the way for new treatment strategies in the field of psychiatry.
Reference
Forebrain EAAT3 overexpression increases susceptibility to amphetamine-induced repetitive behaviors
Jared M. Kopelman, Muhammad O. Chohan, Alex I. Hsu, Eric A. Yttri, Jeremy Veenstra-VanderWeele, and Susanne E. Ahmari
