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 language | English (US) |
|---|---|
| Pages (from-to) | 330-334 |
| Number of pages | 5 |
| Journal | Trends in Neurosciences |
| Volume | 24 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 1 2001 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Psychosis : Pathological activation of limbic thalamocortical circuits by psychomimetics and schizophrenia? / Sharp, Frank R; Tomitaka, M.; Bernaudin, M.; Tomitaka, S.
In: Trends in Neurosciences, Vol. 24, No. 6, 01.06.2001, p. 330-334.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Psychosis
T2 - Pathological activation of limbic thalamocortical circuits by psychomimetics and schizophrenia?
AU - Sharp, Frank R
AU - Tomitaka, M.
AU - Bernaudin, M.
AU - Tomitaka, S.
PY - 2001/6/1
Y1 - 2001/6/1
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0035370757&partnerID=8YFLogxK
U2 - 10.1016/S0166-2236(00)01817-8
DO - 10.1016/S0166-2236(00)01817-8
M3 - Article
VL - 24
SP - 330
EP - 334
JO - Trends in Neurosciences
JF - Trends in Neurosciences
SN - 0378-5912
IS - 6
ER -