期刊
JOURNAL OF COGNITIVE NEUROSCIENCE
卷 22, 期 7, 页码 1452-1464出版社
M I T PRESS
DOI: 10.1162/jocn.2009.21305
关键词
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资金
- NIH Conte Center [MH-064045064045, R01 DA023210-01]
Ketamine, an N-methyl-D-aspartate (NMDA) receptor glutamatergic antagonist, has been studied as a model of schizophrenia when applied in subanesthetic doses. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complex manner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background net-work activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors inmediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia.
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