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VIBRISSAL MOTOR CORTEX (vM1) REORGANIZATION AFTER CORTICAL MOTOR LESION IN THE OPPOSITE HEMISPHERE.
No full textThe 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, p0.05 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
Plastic changes in the vibrissa motor cortex in adult rats after output suppression in the homotopic cortex
No full textAfter motor cortex damage, the unaffected homotopic cortex shows changes in motor output. The present experiments were designed to clarify the nature of these interhemispheric effects. We investigate the vibrissa motor cortex (VMC) output after activity suppression of the homotopic area in adult rats. Comparison was made of VMC output after lidocaine inactivation (L-group) or quinolinic acid lesion (Q-group) of the homotopic cortex. In the Q-group, VMC mapping was performed 3 days (Q3Ds group), 2 weeks (Q2Ws group) and 4 weeks (Q4Ws group) after cortical lesion. In each animal, VMC output was assessed by mapping movements induced by intracortical microstimulation (ICMS) in both hemispheres (hemisphere ipsilateral and contralateral to injections). Findings demonstrated that, in the L-group, the size of vibrissal representation was 39.5% smaller and thresholds required to evoke vibrissa movement were 46.3% higher than those in the Control group. There was an increase in the percentage of ineffective sites within the medial part of the VMC and an increase in the percentage of forelimb sites within the lateral part. Both the Q3Ds group and the L-group led to a similar VMC reorganization (Q3Ds vs. L-group, P > 0.05). In the Q2Ws group the VMC representation showed improvement in size (83.4% recovery compared with controls). The VMC showed recovery to normal output at 4 weeks after lesion (Control vs. Q4Ws group, P > 0.05). These results suggest that the VMC of the two hemispheres continuously interact through excitatory influences, preserving the normal output and inhibitory influences defining the border with the forelimb representation
VIBRISSAL MOTOR CORTEX SHORT-TERM PLASTICITY AFTER HOMOTOPIC CORTEX INACTIVATION IN ADULT RATS
No full textA 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
Whisker motor cortex reorganization after superior colliculus output suppression in adult rats
No full textThe effect of unilateral superior colliculus (SC) output suppression on the ipsilateral whisker motor cortex (WMC) was studied at different time points after tetrodotoxin and quinolinic acid injections, in adult rats. The WMC output was assessed by mapping the movement evoked by intracortical microstimulation (ICMS) and by recording the ICMS-evoked electromyographic (EMG) responses from contralateral whisker muscles. At 1 h after SC injections, the WMC showed: (i) a strong decrease in contralateral whisker sites, (ii) a strong increase in ipsilateral whisker sites and in ineffective sites, and (iii) a strong increase in threshold current values. At 6 h after injections, the WMC size had shrunk to 60% of the control value and forelimb representation had expanded into the lateral part of the normal WMC. Thereafter, the size of the WMC recovered, returning to nearly normal 12 h later (94% of control) and persisted unchanged over time (1-3 weeks). The ICMS-evoked EMG response area decreased at 1 h after SC lesion and had recovered its baseline value 12 h later. Conversely, the latency of ICMS-evoked EMG responses had increased by 1 h and continued to increase for as long as 3 weeks following the lesion. These findings provide physiological evidence that SC output suppression persistently withdrew the direct excitatory drive from whisker motoneurons and induced changes in the WMC. We suggest that the changes in the WMC are a form of reversible short-term reorganization that is induced by SC lesion. The persistent latency increase in the ICMS-evoked EMG response suggested that the recovery of basic WMC excitability did not take place with the recovery of normal explorative behaviou
SUPERIOR COLLICULUS SELECTIVE LESION NOT AFFECT VIBRISSA MOTOR CORTEX OUTPUT IN ADULT RATS.
No full textThe effect of unilateral selective lesion of the superior colliculus (SC) on Vibrissa Motor Cortex (VMC) organization was studied in adult Rats 72 hours (72Hs-group, n=5) and 3 weeks (3Ws-group, n=5) after quinolinic acid lesion. VMC output was assessed mapping the representation size and thresholds of movement evoked by intracortical microstimulation (ICMS). Under ketamine anaesthesia (50mg\Kg i.p.), the ICMS (30 ms trains of 0.25 ms cathodal pulses at 350 Hz, stimulation current 0.05, forelimb sites distribution: 2= 8.63, P>0.05 chi-square test); c) no difference in the mean threshold value required to evoke movements (vibrissa mean threshold in Control-group vs. 72Hs-gorup vs. 3Ws-group: 20.97±2.53μA vs 18.8±2.09μA vs 18.98±1.47μA; forelimb mean threshold in Control-group vs. 72Hs-gorup vs. 3Ws-group: 21.26±2.14μA vs. 19.37±1.35μA vs. 18.64±1.87μA; P>0.05, ANOVA). We conclude that the selective lesion of the SC does not result in any modification in the ipsilateral VMC output. This datum supports the conclusion that the circuitry involved in the cortical regulation of vibrissae movement does not just have one functional prevailing serial pathway but is implemented upon reticular formation and other brain stem nuclei in parallel to the SC
SHORT-TERM FORELIMB MOTOR CORTEX (FM1) PLASTICITY AFTER INACTIVATION OF THE CORRESPONDING CORTEX IN THE OPPOSITE HEMISPHERE
No full textAim: In the primary motor cortex (M1) of adult mammals, electrophysiological changes which are behind the interhemispheric diaschisis remain unclear. In the present study we aimed to demonstrate rapid changes in the M1 forelimb movement representation as the effect of inactivation of the homotopic cortical region.
Methods: Five adult rats underwent three injections of Lidocaine (L-group) within the FM1 of one hemisphere (10μL delivered through a Hamilton syringe at a depth of 1mm from the pial surface). After injections, rats underwent intracortical microstimulation (ICMS) for M1 mapping in both hemispheres. Under ketamine anaesthesia (50mg\Kg i.p.), ICMS (30ms trains of 0.2ms cathodal pulses at 300Hz, stimulation current ≤ 60μA ) was delivered at a depth of 1.5mm from the pial surface using glass-insulated tungsten microelettrodes (impedance:0.6-1.2 ΩM). Other 5 rats were used as Sham-group and 5 rats were used as Control-group.
Results: The cortical area that elicits forelimb movement was analyzed in the hemisphere contralateral to lidocaine injections. We observed significant increase in the forelimb area in the L-group as compared to Sham and Control- group (P<0.005, ANOVA). The forelimb area in L-group expanded in the medial direction overlapping the lateral portion of the vibrissa representation. In this part of M1, the ICMS evoked forelimb and vibrissa movement at the same current threshold. These dual movement sites increase significantly in L-group rats relative to Control and Sham- group of rats (P<0.001, ANOVA).
Conclusions: Our results suggest that FM1 inactivation leads to shaping and size changes of forelimb movement representation in the contralateral hemisphere. We conclude that the loss of the inhibitory interhemispheric input induces the loss of the sharp border between vibrissa and forelimb representation
Suppression of activity in the forelimb motor cortex temporarily enlarges forelimb representation in the homotopic cortex in adult rats.
No full textAfter 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 forelimb motor cortex (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, three days (Q3D group) and two 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). 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 rostro-caudal border between the forelimb and vibrissa representation. This form of interhemispheric diaschisis had completely reversed, with the recovery of the baseline map, 3 days after the lesion in the contalatreral 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
Postnatal development of vibrissae motor output following neonatal infraorbital nerve manipulation
No full textUsing the model of infraorbital nerve (IoN) injury, we have studied the role IoN signals have on the developing vibrissal motor system. To this end, in ten rats, the IoN was severed on the day of birth: in five rats, the IoN was repaired to promote axon regeneration (Reinnervated group) while axon regeneration was prevented in the remaining five rats (Deafferented group). In another five rats, the isolated IoN was left intact (Sham group) and still another group of five rats was left untouched (Control group). After these rats had reached adulthood, the compound muscle action potential (MAP) was recorded from the vibrissa muscle and intracortical microstimulation (ICMS)-evoked movements were mapped in the frontal cortex contralateral to the operated side. We found: (i) no difference between Control, Sham and Reinnervated groups in the integrated MAPs and in the size and excitability of the M1 vibrissal representation. (ii) the Deafferented group showed a 42.9% decrease in the integrated MAP plus a 47.2% and 36.9% reduction, respectively, in the size and excitability of the M1 vibrissae representation. We conclude that, during perinatal life, IoN signals regulate the development of both the peripheral and central vibrissal motor system and that IoN reinnervation restores sensory signals able to stabilize normal development of the vibrissal motor system
The vibrissal motor output following severing and repair of the facial nerve in the newborn rat reorganises less than in the adult
No full textThis study examined the ability of facial motoneurons and motor cortex to reorganise their relationship with the somatic musculature following the severing and repair of the facial nerve in rats at birth. In each adult rat, the organisation of the facial nucleus and the cortical motor output corresponding to the normal side were compared with those corresponding to the reinnervated side. Labelling was used to reveal reinnervation-induced long-term changes in the motoneuron pool supplying vibrissal muscles. Cortical motor output was assessed by mapping the vibrissal movement area extension and thresholds evoked by intracortical microstimulation. After facial nerve reinnervation: (i) the proportion of labelled cell profiles decreased by 85.2% of that in the control side and cortical representation of vibrissal movement decreased by 66.3% of that in control hemispheres; (ii) the reorganised vibrissal representation was shrunken to the medialmost portion of the normal vibrissal representation and there was a medial extension of the forelimb representation, and a more modest lateral extension of eye representation, into the vibrissal territory; (iii) the normal pattern of contralateral vibrissal movement was observed in only 10% of the vibrissal sites, whereas ipsilateral vibrissal movement was found in 53% of the vibrissal sites; (iv) there was an increase in the mean threshold required to evoke contralateral vibrissal movement (32.5 ± 11.1 vs. 20.5 ± 6.9 μA). Thresholds to evoke other types of movement were similar to normal. These changes indicate that an incomplete motor axon regeneration at birth does not restore normal innervation and normal cortical control over the vibrissal muscles
Superior electrochemical performance of carbon nanotubes directly grown on sharp microelectrodes
No full textWe report for the first time how coatings made by directly growing carbon nanotubes (CNTs) on the tip of neural microelectrodes outperform others made by electrodeposited CNT composites. Not only do they reduce microelectrode impedance but they also are able to inject high currents without degradation and are stable in time. These results suggest that they are excellent candidates for chronic applications especially when both neural recording and stimulation have to be performed by the same microelectrode
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