Stroke and traumatic brain injury are the leading cause of adult disability. Motor deficits including spasticity, gait and posture asymmetry, and balance problems are very common. Little is known about underlying mechanisms and there is no effective treatment to facilitate functional recovery and prevent progression of physical disabilities. The dogma in neurology is that motor deficits secondary to brain trauma arise due to aberrant activity of neural pathways descending from the brain to spinal cord. Previous studies in the group challenge this paradigm by the demonstration that signaling from the injured brain to the spinal hindlimb motor circuits is also mediated by the humoral system. The renin–angiotensin system, is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance. Evidence demonstrates that this system has a role in the CNS, is asymmetrically distributed in the CNS, and may regulate lateralized processes. We hypothesize that the brain injury-induced asymmetric hindlimb motor deficit is mediated at least partially through the renin–angiotensin system. Aim of the study is to assess whether expression of genes of the renin–angiotensin system is lateralized in the hypothalamus where it may control other neurohormonal systems, and whether it is affected by the unilateral brain injury. Approach: In this study we will examine if genes of the renin–angiotensin system are targeted in the hypothalamus by unilateral brain injury using quantitative Real-Time polymerase chain reaction (qRT-PCR), and if they are co-expressed with neuroplasticity related genes and other neurohormonal genes. Experimental testing of our hypothesis would shed light on pathogenesis of motor deficits and may open up new treatment options for stroke and traumatic brain injury.