Changes of Functional Connectivity of the Hippocampus in Ketamine-induced Schizophrenic Rat Model.
- Author:
Maan Gee LEE
1
Author Information
1. Department of Pharmacology, School of Medicine, Kyungpook National University, Taegu, Korea. mglee@bh.kyungpook.ac.kr
- Publication Type:Original Article
- Keywords:
Ketamine;
Hippocampus;
NMDA;
Schizophrenia;
EEG;
Functional connectivity
- MeSH:
Anesthesia;
Animals;
Electrodes;
Electroencephalography;
Glutamic Acid;
Hippocampus*;
Humans;
Ketamine;
Male;
Models, Animal*;
N-Methylaspartate;
Rats*;
Schizophrenia;
Synaptic Transmission
- From:Korean Journal of Psychopharmacology
1998;9(1):58-66
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
It has been proposed that the schizophrenic symptoms may be emerged from the dysfunctional connection and abnormal glutamate neurotransmission between prefrontal and temporolimbic cortex. Thus, we examined the functional connectivity between entorhinal cortex-hippocampus in the schizophrenic animal model induced by the NMDA receptor channel blocker, ketamine. Under ketamine+xylazine anesthesia, the electrodes for recording and stimulating were implanted into the hippocampus of the male rat. Recording of EEG and EP was started 3 or more days after operation in 3 different behavioral states (normal mobile and immobile, and ketamine-injected). Each hippocampal area had a characteristic EP. While it did not produce changes on the normal EPs, ketamine produced greater changes on the normal EEG : prominant theta in normal mobile state ; fast and irregular wave accompanying with 1-2 Hz spikes in normal immobile states and ; fAst and irregular rhythm with spindles of 2.5 Hz and 30 Hz which were prominant on DG and CA3 in ketamine-injected state. Log scale of spectrum showed that ketamine increased the power of 6-8 Hz band on CA1 radiatum and of the band over 25 Hz on DG. Also ketamine disrupted the correlated electrical activity among several hippocampal areas. These results may suggest that the symptom of schizophrenics is emerged from reduction of correlated activity but increase of irregular activity over the cortical area and uncontrolled input which is mediated by NMDA receptor.
