Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing.

Sofya P. Kulikova, Elena A. Tolmacheva, Paul Anderson, Julien Gaudias, Brendan Adams, Thomas Zheng, Didier Pinault

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Sensory and cognitive deficits are common in schizophrenia. They are associated with abnormal brain rhythms, including disturbances in 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.
Original languageEnglish
Pages (from-to)3407-3419
Number of pages13
JournalEuropean Journal of Neuroscience
Volume36
Issue number10
DOIs
Publication statusPublished - Nov 2012

Fingerprint

Deep Brain Stimulation
Ketamine
Automatic Data Processing
Electric Stimulation
Aptitude
N-Methyl-D-Aspartate Receptors
Vibrissae
Investigational Therapies
Neuronal Plasticity
Thalamus
Glutamic Acid
Schizophrenia
Injections
Brain

Cite this

Kulikova, Sofya P. ; Tolmacheva, Elena A. ; Anderson, Paul ; Gaudias, Julien ; Adams, Brendan ; Zheng, Thomas ; Pinault, Didier. / Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing. In: European Journal of Neuroscience. 2012 ; Vol. 36, No. 10. pp. 3407-3419.
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abstract = "Sensory and cognitive deficits are common in schizophrenia. They are associated with abnormal brain rhythms, including disturbances in 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.",
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Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing. / Kulikova, Sofya P.; Tolmacheva, Elena A.; Anderson, Paul; Gaudias, Julien; Adams, Brendan; Zheng, Thomas; Pinault, Didier.

In: European Journal of Neuroscience, Vol. 36, No. 10, 11.2012, p. 3407-3419.

Research output: Contribution to journalArticle

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AU - Tolmacheva, Elena A.

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AU - Adams, Brendan

AU - Zheng, Thomas

AU - Pinault, Didier

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KW - High-frequency electrical stimulation

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