Why sigma-1 receptor dysfunction might confer vulnerability to cannabis-induced psychosis
Jonathon Carl Arnold
The International Journal of Neuropsychopharmacology August 13, 2014 DOI: 10.1017/s1461145714000960 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Topics | Cannabis |
| Citations | 1 |
| Key points | Argues that NMDA receptor dysfunction is implicated in schizophrenia, citing evidence that NMDA receptor antagonists induce psychotic states in humans and schizophrenia-relevant behaviour in rodents, and that schizophrenia brain tissue shows reduced NMDA receptor expression and function. Contends that cannabis increases psychosis risk in vulnerable individuals but that the molecular basis of this susceptibility is poorly understood. |
Abstract
The N-methyl-D-aspartate (NMDA) receptor has long been implicated in the pathophysiology of schizophrenia. NMDA receptor antagonists induce psychotic states in humans and when administered to rodents promote lasting behavioural phenotypes relevant to schizophrenia (Javitt and Zukin, 1991; Abi-Saab et al. , 1998; Javitt, 2007). Further, schizophrenia brain tissue contains reduced expression and function of NMDA receptors (Errico et al. , 2013). It is well established that the use of cannabis increases the risk of psychosis in vulnerable individuals; however, our understanding of the molecular basis of this susceptibility is limited.