Format

Send to

Choose Destination
Biol Psychiatry. 2008 Apr 15;63(8):730-5. Epub 2007 Nov 26.

N-methyl d-aspartate receptor antagonists ketamine and MK-801 induce wake-related aberrant gamma oscillations in the rat neocortex.

Author information

1
INSERM U666, Physiopathologie Clinique et Expérimentale de la Schizophrénie, Faculté de Médecine, Strasbourg, France. pinault@neurochem.u-strasbg.fr

Abstract

BACKGROUND:

Single subanesthetic doses of ketamine, a non-competitive NMDA receptor (NMDAr) antagonist, induce cognitive impairment, schizophreniform psychosis, hallucinations, and exacerbate schizophrenia symptoms. The neuronal mechanisms underlying transient disruption in NMDAr function are unknown. Disorders of cognition-related coherences of gamma frequency (30-80 Hz) oscillations between cortical areas are a major functional abnormality in schizophrenic patients. Does a single subanesthetic dose of ketamine or MK-801 alter properties of cortical gamma oscillations?

METHODS:

Properties of spontaneously occurring gamma oscillations in the electrocorticogram of the neocortex of freely moving rats (n = 16) were measured before and after subcutaneous administration of a single dose of ketamine (< or = 10 mg/kg), MK-801 (< or = .16 mg/kg), d-amphetamine (< or = 1 mg/kg), apomorphine (< or = 1.6 mg/kg), or vehicle (sodium chloride, .9%).

RESULTS:

The present study gives the first evidence that ketamine and MK-801, both of which induce NMDAr-dependent functional disconnections, dose-dependently increase the power (200%-400%) of wake-related gamma oscillations in the neocortex. Substances that modulate dopaminergic neurotransmission could also increase the gamma power but to a lesser degree.

CONCLUSIONS:

The present findings suggest that abnormal increased synchronization in ongoing gamma oscillations in cortical-related networks might cause dysfunctions of conscious integration, as seen in patients with schizophrenia.

PMID:
18022604
DOI:
10.1016/j.biopsych.2007.10.006
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center