Present addresses: NEUROSPIN, CEA-Saclay, 91191, Gif sur Yvette, France.
Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing
Article first published online: 29 AUG 2012
© 2012 The Authors. European Journal of Neuroscience © 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 36, Issue 10, pages 3407–3419, November 2012
How to Cite
Kulikova, S. P., Tolmacheva, E. A., Anderson, P., Gaudias, J., Adams, B. E., Zheng, T. and Pinault, D. (2012), Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing. European Journal of Neuroscience, 36: 3407–3419. doi: 10.1111/j.1460-9568.2012.08263.x
- Issue published online: 19 NOV 2012
- Article first published online: 29 AUG 2012
- Received 1 March 2012, revised 10 July 2012, accepted 19 July 2012
- gamma oscillations;
- high-frequency electrical stimulation;
- sensory-evoked potential
Sensory and cognitive deficits are common in schizophrenia. They are associated with abnormal brain rhythms, including disturbances in γ frequency (30–80 Hz) oscillations (GFO) in cortex-related networks. However, the underlying anatomofunctional mechanisms remain elusive. Clinical and experimental evidence suggests that these deficits result from a hyporegulation of glutamate N-methyl-D-aspartate receptors. Here we modeled these deficits in rats with ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist and a translational psychotomimetic substance at subanesthetic doses. We tested the hypothesis that ketamine-induced sensory deficits involve an impairment of the ability of the thalamocortical (TC) system to discriminate the relevant information from the baseline activity. Furthermore, we wanted to assess whether ketamine disrupts synaptic plasticity in TC systems. We conducted multisite network recordings in the rat somatosensory TC system, natural stimulation of the vibrissae and high-frequency electrical stimulation (HFS) of the thalamus. A single systemic injection of ketamine increased the amount of baseline GFO, reduced the amplitude of the sensory-evoked TC response and decreased the power of the sensory-evoked GFO. Furthermore, cortical application of ketamine elicited local and distant increases in baseline GFO. The ketamine effects were transient. Unexpectedly, HFS of the TC pathway had opposite actions. In conclusion, ketamine and thalamic HFS have opposite effects on the ability of the somatosensory TC system to discriminate the sensory-evoked response from the baseline GFO during information processing. Investigating the link between the state and function of the TC system may conceptually be a key strategy to design innovative therapies against neuropsychiatric disorders.