Abstract
Obsessive compulsive disorder (OCD) is a heterogeneous psychiatric disorder affecting 1%–3% of the population worldwide. About half of OCD afflicted individuals do not respond to currently available pharmacotherapy, which is mainly based on serotonin reuptake inhibition. Therefore, there is a critical need to search novel and improved therapeutic targets to treat this devastating disorder. In recent years, accumulating evidence has supported the glutamatergic hypothesis of OCD, and particularly pointing a potential role for the neuronal glutamate transporter EAAT3. This mini-review summarizes recent findings regarding the neurobiological basis of OCD, with an emphasis on the glutamatergic neurotransmission and EAAT3 as a key player in OCD etiology.
Highlights
Reviewed by: Marcela Julio-Pieper, Pontificia Universidad Católica de Valparaíso, Chile Renae Ryan, University of Sydney, Australia
This mini-review summarizes recent findings regarding the neurobiological basis of Obsessive compulsive disorder (OCD), with an emphasis on the glutamatergic neurotransmission and encoding the neuronal glutamate transporter 3 (EAAT3) as a key player in OCD etiology
The Sapap3 KO (Welch et al, 2007) mice, the Slitrk5 KO mice (Shmelkov et al, 2010), and the EAAT3 overexpressing mice (Delgado-Acevedo et al, 2019), have been reported to recapitulate OCD hallmarks including cortico-striatal glutamatergic alterations, changes in NMDA receptors (NMDAR) function, and displaying OCD-like behaviors that could be rescued by chronic administration of SSRI (See Table 1)
Summary
Obsessive compulsive disorder (OCD) is a psychiatric disorder affecting 1%–3% of the population worldwide (Grabe et al, 2000; Angst et al, 2004). Most OCD patients have high levels of anxiety, likely due to the inability to control or stop the appearance of obsessions (Pauls et al, 2014). Both obsessions and compulsions are time consuming, causing a high impairment in social and occupational areas (American Psychiatric Association, 2013). Hyperactivity of the anterior cingulate, orbitofrontal cortex, and caudate (Saxena et al, 2001; Maia et al, 2008), as well as altered functional connectivity between the medial frontal cortex and striatal regions have been reported in OCD (Fitzgerald et al, 2011; Posner et al, 2014)
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