Psychosis: pathological activation of limbic thalamocortical circuits by psychomimetics and schizophrenia?
Trends in neurosciences June 1, 2001 F R Sharp, M Tomitaka, M Bernaudin et al.
Non-competitive NMDA receptor antagonists like phencyclidine, ketamine, and MK801 cause psychosis in humans and damage the cingulate-retrosplenial cortex in adult rodents. This damage can be prevented by GABA-receptor agonists and antipsychotics such as haloperidol and clozapine. Injecting MK801 into the anterior thalamus reproduces the cortical injury, while injecting GABA-receptor agonists there prevents injury from systemic MK801. The authors suggest that inhibiting NMDA receptors on GABAergic thalamic reticular nucleus neurons may activate thalamocortical circuits that cause injury in animals and psychosis in humans, potentially contributing to schizophrenia.