Psychosis: Pathological activation of limbic thalamocortical circuits by psychomimetics and schizophrenia?

Frank R Sharp, M. Tomitaka, M. Bernaudin, S. Tomitaka

Research output: Contribution to journalArticlepeer-review

137 Scopus citations

Abstract

Non-competitive NMDA receptor antagonists, such as phencyclidine, ketamine and MK801, produce psychosis in humans. These drugs also produce injury to cingulate-retrosplenial cortex in adult rodents that can be prevented by GABA-receptor agonists and antipsychotics such as haloperidol and clozapine. MK801 injections into anterior thalamus reproduce limbic cortex injury, and GABA-receptor agonist injections into anterior thalamus prevent injury produced by systemic MK801. Inhibition of NMDA receptors on GABAergic thalamic reticular nucleus neurons might activate thalamocortical 'injury' circuits in animals. Pathological activation of thalamocortical circuits might also mediate the psychosis produced by NMDA-receptor antagonists in humans, and might contribute to psychosis in schizophrenia.

Original languageEnglish (US)
Pages (from-to)330-334
Number of pages5
JournalTrends in Neurosciences
Volume24
Issue number6
DOIs
StatePublished - Jun 1 2001
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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