Peripheral nerve injury influences the disinhibition induced by focal ischaemia in the rat motor cortex
T Farkas, E Racekova, Z Kis, S Horváth, J Burda… - Neuroscience …, 2003 - Elsevier
T Farkas, E Racekova, Z Kis, S Horváth, J Burda, J Galik, J Toldi
Neuroscience letters, 2003•ElsevierPhotothrombotic lesions were produced in the rat primary motor cortex, and the brain
excitability was assessed in a paired-pulse stimulation protocol by transcranial recording, in
parallel at 16 points of the frontal cortex, including the insulted and the surrounding areas.
The cortical lesion reduced the inhibition in the extended frontal cortex, with a delay of a few
minutes. Unilateral facial nerve transection, however, accelerated the widespread
disinhibition. Although the mechanism is not clear in detail, both peripheral and central …
excitability was assessed in a paired-pulse stimulation protocol by transcranial recording, in
parallel at 16 points of the frontal cortex, including the insulted and the surrounding areas.
The cortical lesion reduced the inhibition in the extended frontal cortex, with a delay of a few
minutes. Unilateral facial nerve transection, however, accelerated the widespread
disinhibition. Although the mechanism is not clear in detail, both peripheral and central …
Photothrombotic lesions were produced in the rat primary motor cortex, and the brain excitability was assessed in a paired-pulse stimulation protocol by transcranial recording, in parallel at 16 points of the frontal cortex, including the insulted and the surrounding areas. The cortical lesion reduced the inhibition in the extended frontal cortex, with a delay of a few minutes. Unilateral facial nerve transection, however, accelerated the widespread disinhibition. Although the mechanism is not clear in detail, both peripheral and central injury-induced disinhibition may have a significant impact on the recovery of the function.
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