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Whisker motor cortex reorganization after superior colliculus output suppression in adult rats
Author(s) -
Veronesi Carlo,
Maggiolini Emma,
Franchi Gianfranco
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12322
Subject(s) - superior colliculus , lesion , motor cortex , neuroscience , excitatory postsynaptic potential , electromyography , microstimulation , anatomy , psychology , chemistry , medicine , inhibitory postsynaptic potential , stimulation , surgery
The 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 behaviour.