RESUMEN
Patients with sickle cell disease (SCD) have been shown to have impaired visual-motor speed and coordination. Sensorimotor deficits in mice can be investigated by motor coordination tests that require whole body movements such as the rotorod. A sickle transgenic mouse model (S+S-Antilles) that expresses human alpha, human beta(S) and human beta(S-Antilles), is homozygous for the mouse beta(major) deletion, and has low plasma arginine was compared to control C57BL/6J mice and S+S-Antilles mice supplemented with 5% arginine on the rotorod. The rotorod consists of a 2.5 cm diameter, grooved rod turning at constant acceleration, requiring postural adjustments on the part of the mice to maintain equilibrium. C57BL mice on Purina mouse chow had an average latency to fall of S+S-Antilles mice on Purina mouse chow had an average of 127+/-56 s S+S-Antilles mice after 5% arginine supplementation had a mean latency of Arginine may improve rotorod performance in sickle transgenic mice by increasing NO synthesis thereby improving vasodilatation and blood flow with reversal of ischemia in brain and/or muscle. In conclusion, impaired rotorod performance in sickle transgenic mice presents an opportunity to apply this simple task to provide an efficient method to screen some types of therapeutic regimens for efficacy in SCD.