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Lesions of the vestibular system disrupt hippocampal theta rhythm in the rat.

Full Abstract

The hippocampus has a major role in memory for spatial location. Theta is a rhythmic hippocampal EEG oscillation that occurs at approximately 8 Hz during voluntary movement and that may have some role in encoding spatial information. We investigated whether, as part of this process, theta might be influenced by self-movement signals provided by the vestibular system. The effects of bilateral peripheral vestibular lesions, made > or = 60 days prior to recording, were assessed in freely moving rats. Power spectral analysis revealed that theta in the lesioned animals had a lower power and frequency compared with that recorded in the control animals. When the electroencephalography (EEG) was compared in epochs matched for speed of movement and acceleration, theta was less rhythmic in the lesioned group, indicating that the effect was not a result of between-group differences in this behavior. Blood measurements of corticosterone were also similar in the two groups indicating that the results could not be attributed to changes in stress levels. Despite the changes in theta EEG, individual neurons in the CA1 region of lesioned animals continued to fire with a periodicity of approximately 8 Hz. The positive correlation between cell firing rate and movement velocity that is observed in CA1 neurons of normal animals was also maintained in cells recorded from lesion group animals. These findings indicate that although vestibular signals may contribute to theta rhythm generation, velocity-related firing in hippocampal neurons is dependent on nonvestibular signals such as sensory flow, proprioception, or motor efference copy.

 

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Author information

Author/s: Russell, Noah A (NA); Horii, Arata (A); Smith, Paul F (PF); Darlington, Cynthia L (CL); Bilkey, David K (DK);

Affiliation: Department of Psychology, School of Medical Sciences, University of Otago, Dunedin, New Zealand.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Journal of neurophysiology (J Neurophysiol), published in United States. (Language: eng)

Reference: 2006-Jul; vol 96 (issue 1) : pp 4-14

Dates: Created 2006/06/14; Completed 2006/08/04; Revised 2007/11/15;

PMID: 16772515, status: MEDLINE (last retrieval date: 12/26/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

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Associated Chemicals: Corticosterone (50-22-6)

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