VIBRISSAL MOTOR CORTEX SHORT-TERM PLASTICITY AFTER HOMOTOPIC CORTEX INACTIVATION IN ADULT RATS

A large number of reports point out to functional and structural changes of motor cortex as the effect of the injury in the corresponding region in the opposite hemisphere (homotopic cortex). Nevertheless in the non-damaged hemisphere, the nature of electrophysiological changes remains unclear. In rats, the organization of the vibrissal motor system is bilateral and the vibrissa motor cortex (VMC) is an area rich in interhemispheric connections. The purpose of the present study was to investigate the short-term reorganization of the VMC after inactivation of the homotopic cortex. To this end, 7 adult rats underwent injections of Lidocaine 3% (15 μL ) (L-group) delivered through a Hamilton syringe at a depth of 1mm from the pial surface into three different sites within the left VMC (Coordinate in mm: Bregma +1, L +1; Bregma +2, L+1,5 and Bregma +3, L1,5). Rats underwent intracortical microstimulation (ICMS) for VMC mapping in both hemispheres after VMC inactivation in one hemisphere. Moreover, VMC mapping was performed in both hemispheres in Control-(n=5) and Sham-group (n=5) of rats. Under ketamine anaesthesia (50mg\Kg i.p.) the ICMS (30 ms trains of 0.2 ms cathodal pulses at 300 Hz, stimulation current ≤60μA) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2MΩ). There was no difference in VMC output in Control vs. Sham-group (p>0.05). In the L-group, in comparison with Control one, a significant shrinkage of the VMC size and a significant decrease of the VMC excitability was observed (mean size L-group: 2.3±0.8mm2 vs. Control: 3.8±0.6mm2, p<0.0007; mean threshold for vibrissa movement in L-group: 29.4±4.1μA vs. Control: 20.7±1.9μA, p<0.0008 ANOVA). These results suggest that the VMC of the two hemispheres continuously interact through excitatory influences for maintaining normal VCM output.