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J Neurophysiol 89: 2380-2388, 2003. First published January 15, 2003; doi:10.1152/jn.01098.2002
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J Neurophysiol (May 1, 2003). 10.1152/jn.01098.2002
Submitted on Submitted 6 December 2002; accepted in final form 13 January 2003

Effects of Ventrobasal Lesion and Cortical Cooling on Fast Oscillations (>200 Hz) in Rat Somatosensory Cortex

Richard J. Staba, Barbara Brett-Green, Marcy Paulsen, and Daniel S. Barth

Department of Psychology, University of Colorado, Boulder, Colorado 80309

Staba, Richard J., Barbara Brett-Green, Marcy Paulsen, and Daniel S. Barth. Effects of Ventrobasal Lesion and Cortical Cooling on Fast Oscillations (>200 Hz) in Rat Somatosensory Cortex. J. Neurophysiol. 89: 2380-2388, 2003. High-frequency oscillatory activity (>200 Hz) termed "fast oscillations" (FO) have been recorded in the rodent somatosensory cortex and may reflect very rapid integration of vibrissal information in sensory cortex. Yet, while electrophysiological correlates suggest that FO is generated within intracortical networks, contributions of subcortical structures along the trigeminal pathway remain uncertain. Using surface and laminar electrode arrays, in vivo recordings of vibrissal and electrically evoked FO were made within somatosensory cortex of anesthetized rodents before and after ablation of the ventrobasal thalamus (VB) or during reversible cortical cooling. In VB-lesioned animals, vibrissal stimulation failed to evoke FO, while epicortical stimulation in lesioned animals remained effective in generating FO. In nonlesioned animals, cortical cooling eliminated vibrissal-evoked FO despite the persistence of thalamocortical input. Vibrissal-evoked FO returned with the return to physiological temperatures. Results from this study indicate that somatosensory cortex alone is able to initiate and sustain FO. Moreover, these data suggest that cortical network interactions are solely responsible for the generation of FO, while synchronized thalamocortical input serves as the afferent trigger.




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