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 (ION cut) and then the facial nerve (VII cut) 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. M1 output was compared in different types of peripheral manipulations: (i) contralateral intact vibrissal pad (intact hemispheres), (ii) contralateral VII cut (VII hemispheres), (iii) contralateral ION cut (ION hemispheres), (iv) contralateral VII cut after contralateral ION cut (ION + VII hemispheres), (v) contralateral pad botulinum-toxin-injected after ION cut (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 contralateral 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 h 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.
Short-term reorganization of input-deprived motor vibrissae representation following motor disconnection in adult rats
FRANCHI, Gianfranco;VERONESI, Carlo
2006
Abstract
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 (ION cut) and then the facial nerve (VII cut) 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. M1 output was compared in different types of peripheral manipulations: (i) contralateral intact vibrissal pad (intact hemispheres), (ii) contralateral VII cut (VII hemispheres), (iii) contralateral ION cut (ION hemispheres), (iv) contralateral VII cut after contralateral ION cut (ION + VII hemispheres), (v) contralateral pad botulinum-toxin-injected after ION cut (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 contralateral 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 h 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.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
