Suppression of activity in the forelimb motor cortex temporarily enlarges forelimb representation in the homotopic cortex in adult rats.
After forelimb motor cortex (FMC) damage, the unaffected homotopic motor cortex showed plastic changes. The present experiments were designed to clarify the electrophysiological nature of these interhemispheric effects. To this end, the output reorganization of the FMC was investigated after homotopic area activity was suppressed in adult rats. FMC output was compared after lidocaine-induced inactivation (L-group) or quinolinic acid-induced lesion (Q-group) of the contralateral homotopic cortex. In the Q-group of animals, FMC mapping was performed, respectively, 3 days (Q3D group) and 2 weeks (Q2W group) after cortical lesion. In each animal, FMC output was assessed by mapping movements induced by intracortical microstimulation (ICMS) in both hemispheres (hemisphere ipsilateral and contralateral to injections). The findings demonstrated that in the L-group, the size of forelimb representation was 42.2% higher than in the control group (P < 0.0001). The percentage of dual forelimb-vibrissa movement sites significantly increased over the controls (P < 0.0005). The dual-movement sites occupied a strip of the map along the rostrocaudal border between the forelimb and vibrissa representations. This form of interhemispheric diaschisis had completely reversed, with the recovery of the baseline map, 3 days after the lesion in the contralateral FMC. This restored forelimb map showed no ICMS-induced changes 2 weeks after the lesion in the contralateral FMC. The present results suggest that the FMCs in the two hemispheres interact continuously through predominantly inhibitory influences that preserve the forelimb representation and the border vs. vibrissa representation.
Dipartimento di Scienze Biomediche e Terapie Avanzate, Sezione di Fisiologia umana e Istituto Nazionale di Neuroscienze, Università di Ferrara, 44100 Ferrara, Italy.
Emma
E
Maggiolini
Riccardo
R
Viaro
Gianfranco
G
Franchi
D000200:Action Potentials / Q000502:physiology; D000779:Anesthetics, Local; D000818:Animals; D001930:Brain Injuries / Q000139:chemically induced / Q000503:physiopathology; D001931:Brain Mapping; D003714:Denervation; D004292:Dominance, Cerebral / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D004594:Electrophysiology; D005552:Forelimb / Q000294:innervation*; D008012:Lidocaine; D008465:Mechanoreceptors / Q000502:physiology; D008839:Microelectrodes; D009044:Motor Cortex / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D009498:Neurotoxins; D017378:Quinolinic Acid; D051381:Rats; D014738:Vibrissae / Q000294:innervation
D000779:Anesthetics, Local; D009498:Neurotoxins; D008012:Lidocaine; D017378:Quinolinic Acid