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The Journal of Neuroscience, November 12, 2003, 23(32):10378-10387

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Development/Plasticity/Repair
Lesions of Mature Barrel Field Cortex Interfere with Sensory Processing and Plasticity in Connected Areas of the Contralateral Hemisphere

V. Rema and Ford F. Ebner

Department of Psychology, Vanderbilt University, Nashville, Tennessee 37203

Lesions of primary sensory cortex produce impairments in brain function as an outcome of the direct tissue damage. In addition, indirect lesion effects have been described that consist of functional deficits in areas sharing neural connections with the damaged area. The present study characterizes interhemispheric deficits produced as a result of unilateral lesions of the entire vibrissa representation of S-I barrel field cortex (BFC) in adult rats using single-neuron recording under urethane anesthesia. After unilateral lesions of adult BFC, responses of neurons in the contralateral homotopic BFC are severely depressed. Background (spontaneous) activity is reduced by 80%, responses to test stimuli applied to the whiskers are reduced by 50%, and onset of synaptic plasticity induced by trimming all but two whiskers ("whisker-pairing plasticity") is delayed over sevenfold compared with sham-lesion control animals. These deficits persist with only slight improvement for at least 4 months after lesion. Both fast-spiking and regular-spiking neuron responses are diminished contralateral to the lesion, as are cells above, below, and within the cortical barrels. Enriched environment experience increased the magnitude of responses and accelerated the rate of synaptic plasticity but did not restore response magnitude to control levels. Deficiencies in evoked responses and synaptic plasticity are primarily restricted to areas that share direct axonal connections with the lesioned cortex, because equivalently sized lesions of visual cortex produce minimal deficits in contralateral BFC function. These results indicate that interhemispheric deficits consist of remarkable and persistent decrements in sensory processing at the single-neuron level and support the idea that the deficits are somehow linked to the shared neural connections with the area of brain damage.

Key words: cortical lesions; stroke; brain injury; diaschisis; synaptic plasticity; enriched environment

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Received March 14, 2003; revised September 15, 2003; accepted September 15, 2003.

This article has been cited by other articles:

				S. Glazewski, B. L. Benedetti, and A. L. Barth Ipsilateral Whiskers Suppress Experience-Dependent Plasticity in the Barrel Cortex J. Neurosci., April 4, 2007; 27(14): 3910 - 3920. [Abstract] [Full Text] [PDF]

				L. Li, V. Rema, and F. F. Ebner Chronic Suppression of Activity in Barrel Field Cortex Downregulates Sensory Responses in Contralateral Barrel Field Cortex J Neurophysiol, November 1, 2005; 94(5): 3342 - 3356. [Abstract] [Full Text] [PDF]

				C. P. Pluto, N. L. Chiaia, R. W. Rhoades, and R. D. Lane Reducing Contralateral SI Activity Reveals Hindlimb Receptive Fields in the SI Forelimb-Stump Representation of Neonatally Amputated Rats J Neurophysiol, September 1, 2005; 94(3): 1727 - 1732. [Abstract] [Full Text] [PDF]

				M. C. Wiest, N. Bentley, and M. A. L. Nicolelis Heterogeneous Integration of Bilateral Whisker Signals by Neurons in Primary Somatosensory Cortex of Awake Rats J Neurophysiol, May 1, 2005; 93(5): 2966 - 2973. [Abstract] [Full Text] [PDF]

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