RESUMO
Traumatic brain injury (TBI) stands as a prominent global cause of disability, with motor deficits being a common consequence. Despite its widespread impact, the precise pathological mechanisms underlying motor deficits after TBI remain elusive. In this study, hindlimb postural asymmetry (HL-PA) development in rats subjected to focal TBI was investigated to explore the potential roles of collagen IV and laminin within the extracellular matrix (ECM) of selected hindlimb muscles in the emergence of motor deficits following TBI. A focal TBI was induced by ablating the left sensorimotor cortex in rats and motor deficits were assessed by measuring HL-PA. The expression of laminin and collagen IV in eight selected muscles on each side of the hindlimbs from both TBI- and sham-operated rats were studied using immunohistochemistry and semi-quantitatively analyzed. The results indicated that the TBI rats exhibited HL-PA, characterized by flexion of the contralateral (right) hindlimb. In the sham-operated rats, the immunoreactive components of laminin and collagen IV were evenly and smoothly distributed along the border of the muscle fibers in all the investigated muscles. In contrast, in the TBI rats, the pattern was broken into aggregated, granule-like, immunoreactive components. Such a labeling pattern was detected in all the investigated muscles both from the contra- and ipsilateral sides of the TBI rats. However, in TBI rats, most of the muscles from the contralateral hindlimb showed a significantly increased expression of these two proteins in comparison with those from the ipsilateral hindlimb. In comparison to sham-operated rats, there was a significant increase in laminin and collagen IV expression in various contralateral hindlimb muscles in the TBI rats. These findings suggest potential implications of laminin and collagen IV in the development of motor deficits following a focal TBI.
RESUMO
Brain injury and stroke are leading causes of adult disability. Motor deficits are common problems, and their underlying pathological mechanisms remain poorly understood. The serotoninergic system is implicated in both functional recovery from and the occurrence of spasticity after injuries to the central nervous system. This study, which was conducted on rats, investigated the development of limb postural changes and their relationship to the expression of serotonin (5-HT) 2A and 2C receptors in the spinal cord in the 4 weeks after focal traumatic brain injury (TBI) to the right hindlimb sensorimotor cortex. The limb motor deficits were assessed by measuring gait pattern changes during walking and hindlimb postural asymmetry at different time intervals (3−28 days) after surgery. The expressions of the 5-HT2A and 2C receptors in the lumbar spinal cord were investigated using immunohistochemistry. The results showed that all the rats with TBI, independently of the duration of the interval, displayed postural asymmetry with flexion on the contralateral (left) side (>2 mm), while the sham-operated rats showed no apparent postural asymmetry. The TBI rats also had longer stride lengths during walking in both their hindlimbs and their forelimbs compared with the sham rats. For both the TBI and the sham rats, the hind-paw placement angles were larger on the contralateral side in some of the groups. Compared to the sham-operated rats, the 5-HT2A and 2C receptor expression did not significantly change on either side of the lumbar spinal cords of the TBI rats in any of the groups. These results suggest that focal TBI can induce motor deficits lasting a relatively long time, and that these deficits are not related to the expression of the 5-HT2A and 2C receptors in the spinal cord.