Motor Skill Training Promotes Sensorimotor Recovery and Increases Microtubule-Associated Protein-2 (MAP-2) Immunoreactivity in the Motor Cortex after Intracerebral Hemorrhage in the Rat

Abstract

Motor skill learning may induce behavioral and neurophysiological adaptations after intracerebral hemorrhage (ICH). Learning a new motor skill is associated with dendritic reorganization and requires protein synthesis and expression of MAP-2. The purpose of this study was to evaluate motor performance and expression of MAP-2 in the motor cortex of rats submitted to intracerebral hemorrhage model (ICH) and skill task training (SK) or unskilled training (US) during 4 weeks. The Staircase test was used for behavioral evaluation, and relative optical densities and morphometrical analysis were used to estimate MAP-2 immunoreactivity and parameters of brain tissue in both motor cortices. Results show that skill task training performed with the impaired forelimb was able to increase MAP-2 immunoreactivity in the motor cortex either in sham or in ICH groups in both cortices: ipsilesional [F (5,35) = 14.25 (P < 0.01)] and contralesional hemispheres [F (5,35) = 9.70 (P < 0.01)]. ICH alone also increased MAP-2 immunoreactivity despite the absence of functional gains. Behavioral evaluation revealed that ICH-SK group performed better than ICH and ICH-US animals in the Staircase test. Data suggest that motor skill training induces plastic modifications in both motor cortices, either in physiological or pathological conditions and that skill motor training produces higher brain plasticity and positive functional outcomes than unskilled training after experimental intracerebral hemorrhage.

Figure 1

(a) Graphic representation of numbers of pellets consumed. Pellets from the first steps (1st to 4th) and from deeper steps (5th to 7th) over time. S (sham), ICH (intracerebral hemorrhage), SK (skilled training), and US (unskilled training). Data are presented as mean ± standard error (SEM). Dotted line represents minimum criteria of pellets retrieved for inclusion of animals in the study. Data are presented as mean ± standard error (SEM). (b) (A) Representative brain slice stained with MAP-2 showing areas of the interest (AOI) used to determine M1 optical density. (B) Representative area showing MAP-2 staining. (C) Relative optical density of MAP-2 staining in ipsilesional M1: “a” differences between S and S-SK (P < 0.001), ICH (P < 0.02), ICH-SK, and ICH-US (P < 0.001); “b” difference between S-US and ICH-SK (P < 0.001), and ICH-US (P < 0.03); “c” difference between ICH and ICH-SK (P < 0.01). (D) Relative optical density of MAP-2 staining in contralesional M1: “a” difference between S and S-SK, ICH, ICH-SK (P < 0.01), and ICH-US (P < 0.02); “b” difference between S-US and ICH-SK (P < 0.01); “d” difference between ICH-SK and ICH-US (P = 0.04). S (sham), ICH (intracerebral hemorrhage), SK (skilled training), and US (unskilled training). Data are presented as mean ± standard error (SEM).