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Received March 7, 2006
Revised March 27, 2006
Accepted after revision May 9, 2006
1 Dip. di Scienze Biomediche e Terapie Avanzate, Sezione di Fisiologia Umana
* To whom correspondence should be addressed. E-mail: fhg{at}dns.unife.it.
It has been proposed that abnormal vibrissae input to the motor cortex (M1) mediates short-term cortical reorganization after facial nerve lesion. To test this hypothesis we cut first the infraorbital nerve (IONcut) and then the facial nerve (VIIcut) in order to evaluate M1 reorganization without any aberrant, facial nerve-lesion-induced sensory feedback. In each animal, M1 output was assessed in both hemispheres, by mapping movements induced by intracortical microstimulation (ICMS). M1 output was compared in different types of peripheral manipulations: i) contralateral intact vibrissal pad (Intact hemispheres); ii) contralateral VIIcut (VII hemispheres); iii) Contralateral IONcut (ION hemispheres); iv) contralateral VIIcut after contralateral IONcut (ION+VII hemispheres); v) Contralateral pad Botulinum toxin-injected after IONcut (ION+BTX hemispheres). Right and Left hemispheres in untouched animals were the reference for normal M1 map (Control hemispheres). Findings demonstrated that: (1) in ION hemispheres, the mean size of the vibrissae representation was not significantly different from those in Intact and Control hemispheres; (2) reorganization of the vibrissae movement representation clearly emerged only in hemispheres where the contra-lateral vibrissae pad had undergone motor output disconnection (VII cut hemispheres); (3) the persistent loss of vibrissae input did not change the M1 reorganization pattern during the first 48 hours after motor paralysis (ION+VII cut and ION+BTX hemispheres). Thus, after motor paralysis, vibrissa input does not provide the gating signal necessary to trigger M1 reorganization.
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