Traumatic brain injury (TBI) is a well-known cause of disability and mortality worldwide, affecting millions of individuals each year (Faul et al., 2010; Miller et al., 2021). Mild TBI (mTBI) represents >70 % of TBI cases and can cause behavioral, cognitive and motor alterations that can persist for years after the primary insult (Cardoso et al., 2019; Feigin et al., 2013; Lecuyer Giguere et al., 2020).

The striatum, which is an important component of basal ganglia, has connections with the sensorimotor cortex and is related to motor control, learning, and cognitive function (Cataldi et al., 2021; Mello and Villares, 1997). Experimental studies have shown that motor changes were associated with inflammation and oxidative stress in the striatum at 24 h (Huang et al., 2018) and 6 days (Harmon et al., 2017) after moderate to severe TBI in rats. Changes in motor coordination on the rotarod have also been reported (Macks et al., 2022). Whether striatal damage plays a major role in mTBI-related motor impairments remain to be explored.

The Renin-Angiotensin System (RAS) has receptors in key brain areas, including the striatum (Häuser et al., 1998), and has been implicated in TBI outcomes (Janatpour et al., 2019; Khaksari et al., 2018; Machado et al., 2025). Angiotensin II is a major player of the RAS classical arm acting through its AT1 receptors to promote neuroinflammation and oxidative stress. Through the Mas receptors, Angiotensin 1–7, has effects opposite to the AT1 receptors, inducing anti-inflammatory and anti-oxidative actions, thus being recognized as the RAS counter-regulatory arm (Guo et al., 2001; Santos et al., 2003). Pharmacological blockade of the AT1 receptors improved behavior and motor functions after TBI by decreasing neuroinflammation and oxidative stress (Timaru-Kast et al., 2019; Villapol et al., 2015; Xiong et al., 2020; Machado et al., 2025), reinforcing the involvement of the RAS on TBI outcomes. Recently, we demonstrated that an imbalance between the classical and counter-regulatory RAS arms toward the activation of the former in the hippocampus and prefrontal cortex led to motor dysfunction and anxiety-like behavior secondary to mTBI (Machado et al., 2025).

Herein, we investigated the hypothesis that changes in the RAS components alongside inflammation and oxidative stress in the striatum may underlie mTBI-related motor impairments. The current study may broaden our knowledge regarding mTBI pathophysiology and open new opportunities for the development of therapeutic targets focused on mitigating mTBI complications.