The Rat’s vM1 is linked to the corresponding cortex by reciprocal interhemispheric connections. The contribution of these interhemispheric interactions in maintaining normal vM1 output remains to be determined. This study investigates whether the selective lesion of the vM1 leads to functional reorganization of the intact opposite vM1. To this end, 10 adult rats underwent injections of Quinolinic acid (1μL of 60 mM dissolved in 0.1 M phosphate-buffered saline, pH 7.2) delivered through a 1 μL Hamilton syringe at a depth of 1mm from the pial surface into two different sites within the left vM1 (Coordinate in mm: Bregma +1.5, L +1 and Bregma +3, L+1). Rats underwent intracortical microstimulation (ICMS) for right vM1 mapping, 72 hours (72Hs-group, n=5) and 2 weeks (2Ws-group, n=5), after left vM1 lesion. Other 5 rat were used as Control group. Under ketamine anaesthesia (50mg\Kg i.p.) the ICMS (30 ms trains of 0.2 ms cathodal pulses at 300 Hz, stimulation current ≤60 μA) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2MΩ). In the 72Hs-group, in comparison with Control one, a significant shrinkage of the vM1 size and a significant decrease of the vM1 excitability was observed (mean size 72Hs-group: 2.29±0.5mm2 vs. Control: 3.75±0.7mm2; mean threshold for vibrissa movement in 72Hs-group: 25.8±8.3 vs. Control: 20.19±4.3 μA, p<0.05 ANOVA). In contrast, the mean values of the vM1 size and excitability in the 2Ws-group were not significantly different to those in the Control group (p>0.05 ANOVA). Present result suggests a facilitatory role of the interhemispheric input between corresponding vM1 regions. We propose that the S1-barrelfield input to vM1 could drive the recover of the normal vM1 output in time.
VIBRISSAL MOTOR CORTEX (vM1) REORGANIZATION AFTER CORTICAL MOTOR LESION IN THE OPPOSITE HEMISPHERE.
MAGGIOLINI, Emma;FRANCHI, Gianfranco
2005
Abstract
The Rat’s vM1 is linked to the corresponding cortex by reciprocal interhemispheric connections. The contribution of these interhemispheric interactions in maintaining normal vM1 output remains to be determined. This study investigates whether the selective lesion of the vM1 leads to functional reorganization of the intact opposite vM1. To this end, 10 adult rats underwent injections of Quinolinic acid (1μL of 60 mM dissolved in 0.1 M phosphate-buffered saline, pH 7.2) delivered through a 1 μL Hamilton syringe at a depth of 1mm from the pial surface into two different sites within the left vM1 (Coordinate in mm: Bregma +1.5, L +1 and Bregma +3, L+1). Rats underwent intracortical microstimulation (ICMS) for right vM1 mapping, 72 hours (72Hs-group, n=5) and 2 weeks (2Ws-group, n=5), after left vM1 lesion. Other 5 rat were used as Control group. Under ketamine anaesthesia (50mg\Kg i.p.) the ICMS (30 ms trains of 0.2 ms cathodal pulses at 300 Hz, stimulation current ≤60 μA) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2MΩ). In the 72Hs-group, in comparison with Control one, a significant shrinkage of the vM1 size and a significant decrease of the vM1 excitability was observed (mean size 72Hs-group: 2.29±0.5mm2 vs. Control: 3.75±0.7mm2; mean threshold for vibrissa movement in 72Hs-group: 25.8±8.3 vs. Control: 20.19±4.3 μA, p<0.05 ANOVA). In contrast, the mean values of the vM1 size and excitability in the 2Ws-group were not significantly different to those in the Control group (p>0.05 ANOVA). Present result suggests a facilitatory role of the interhemispheric input between corresponding vM1 regions. We propose that the S1-barrelfield input to vM1 could drive the recover of the normal vM1 output in time.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
