Spasticity, characterized by increased spinal stretch reflexes, appears after a certain period following stroke and it is impaired sever skilled movement by spasticity. The mechanism in the cerebral neuronal circuitry is still largely unknown. This present study focused changing of neuronal activity on the ventral medullary reticular nucleus (MdV), which has been recognized as the region associated with skilled movement. Quantitative activation-induced manganese-enhanced MRI is noninvasive measurement of the history of neuronal activity. Manganese ions (Mn2+) enter and accumulate in active neurons via calcium channels. Differential accumulation of Mn2+ is generally assessed using T1 (R1 = T1-1) value. Spasticity in stroke mice was confirmed to attenuate of rate dependent depression of the Hoffman's reflex (H-reflex). The adjusted R1 values in the contralesional MdV among the 1-week post-stroke were significantly upregulated than those in the sham. To detect the neuronal activity relating to spasticity, we investigated the use of electrostimulation of afferent nerve to induce H-reflex. Stimulated mice had significantly increased R1 values in the contralesional MdV of 1-, 2- and 4-week post-stroke than the stimulated sham mice. Interestingly, the R1 values of the sham with electrostimulation were decreased significantly compared to those without electrostimulation. In these results, neuronal activity in contralesional MdV at 1-week post-stroke was significantly elevated and the electrostimulation of afferents generally suppressed neural activity of MdV; however, that of stroke mice significantly elevated neural activity. The present study suggests that abnormal neural activity and neural responses may occur in the MdV associated with skilled movements.