The vibrissa motor cortex (VMC) receives dense excitatory projections from vibrissa barrel cortex (VBC). The contribution of the VBC input to VMC in maintaining normal motor output remains to be determined. This study investigates the early modifications in the VMC after the selective inactivation of the VBC in the same hemisphere. To this end, 5 adult rats underwent injections of mepivacaine (3%, 1 microl) delivered through a 1 microl Hamilton syringe perpendicularly at a depth of 1.5mm from the pial surface into three different sites within the VBC. Rats underwent intracortical microstimulation (ICMS) for mapping VMC ipsilateral to inactivated BFC and to test the inactivation of the injected VBC. To study the effect of the restored drive from VBC to VMC, in the same animals a second mapping session was performed after washout of mepivacaine in VBC. Moreover, VMC and VBC were investigated in Control- (n=5) and Sham-group (three injections of 0,9% saline 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 ≤60 μA) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2MΩ). ICMS experiments demonstrated that, in the ipsilateral VMC there was a decrease both in the size and in excitability of vibrissa representation compared to Control- and Sham-groups (p<0.0001 ANOVA). Within the ipsilateral VMC, also, there was an increase in the percentage: i- of ineffective sites (p<0.005 ANOVA), ii- of forelimb sites (p<0.001) in its lateral part, and iii- of eye sites (p<0.005 ANOVA) in its medial part. After mepivacaine washout in VBC, the vibrissa representation in VMC recovered normal size and excitability (p>0.05, ANOVA). The inhibition of excitatory projections to VMC induces a reduction of size and excitability of the vibrissa representation. A decrease of intracortical inhibition may explain the enlargement of the eye and forelimb representation within the VMC ipsilateral to inactivated BFC. Vibrissal input information processing in cortico-cortical pathway seems critical in the maintaining of normal VMC output.
Reversible modifications in the vibrissa motor cortex after unilateral vibrissa barrel field cortex inactivation in adult rats.
VERONESI, Carlo;FRANCHI, Gianfranco
2009
Abstract
The vibrissa motor cortex (VMC) receives dense excitatory projections from vibrissa barrel cortex (VBC). The contribution of the VBC input to VMC in maintaining normal motor output remains to be determined. This study investigates the early modifications in the VMC after the selective inactivation of the VBC in the same hemisphere. To this end, 5 adult rats underwent injections of mepivacaine (3%, 1 microl) delivered through a 1 microl Hamilton syringe perpendicularly at a depth of 1.5mm from the pial surface into three different sites within the VBC. Rats underwent intracortical microstimulation (ICMS) for mapping VMC ipsilateral to inactivated BFC and to test the inactivation of the injected VBC. To study the effect of the restored drive from VBC to VMC, in the same animals a second mapping session was performed after washout of mepivacaine in VBC. Moreover, VMC and VBC were investigated in Control- (n=5) and Sham-group (three injections of 0,9% saline 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 ≤60 μA) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2MΩ). ICMS experiments demonstrated that, in the ipsilateral VMC there was a decrease both in the size and in excitability of vibrissa representation compared to Control- and Sham-groups (p<0.0001 ANOVA). Within the ipsilateral VMC, also, there was an increase in the percentage: i- of ineffective sites (p<0.005 ANOVA), ii- of forelimb sites (p<0.001) in its lateral part, and iii- of eye sites (p<0.005 ANOVA) in its medial part. After mepivacaine washout in VBC, the vibrissa representation in VMC recovered normal size and excitability (p>0.05, ANOVA). The inhibition of excitatory projections to VMC induces a reduction of size and excitability of the vibrissa representation. A decrease of intracortical inhibition may explain the enlargement of the eye and forelimb representation within the VMC ipsilateral to inactivated BFC. Vibrissal input information processing in cortico-cortical pathway seems critical in the maintaining of normal VMC output.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
