The contribution of the vibrissa barrel field cortex (BFC) input to vibrissa motor cortex (VMC) in maintaining normal motor output remains to be determined. This study investigates the early adaptations in the VMC of both hemispheres after the selective inactivation of the BFC in one hemisphere. To this end, 7 adult rats underwent injections of lidocaine (3%, 2micronl) delivered through a 1 micronl Hamilton syringe perpendicularly at a depth of 1.5mm from the pial surface into three different sites within the BFC. Rats underwent intracortical microstimulation (ICMS) for mapping VMC ipsilateral and contralateral to inactivated BFC. Moreover, VMC output was investigated in Control- (n=5) and Sham-group (three injections of saline, 0, 9%/2micronl, into BFC; n=5). Under ketamine anaesthesia (50mg\Kg i.p.) the ICMS (30 ms trains of 0.2 ms cathodal pulses at 300 Hz, stimulation current lower than 60 microA) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2MOhm). Findings demonstrated that, in the ipsilateral VMC there was a decrease both in the size and in excitability of vibrissa representation compared to Controls (p<0.0001 ANOVA). Within the ipsilateral VMC, also, there was an increase in the percentage of ineffective sites (p<0.005 ANOVA) and in the medial part of the representation, of the eye sites (p<0.005 ANOVA). In the contralateral VMC the decrease in the size and excitability was significant in comparison to Controls (p<0.05 ANOVA) but not as much of than those in the ipsilateral VMC. A loss in intracortical facilitation due to BFC inactivation may explain reduced size and excitability of the VMC in both ipsilateral and contralateral hemisphere. A decrease in the intracortical inhibition may explain the enlarged representation of the eye sites in the VMC ipsilateral to inactivated BFC.
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