Association of medullary reticular formation ventral part with spasticity in mice suffering from photothrombotic stroke

Strokes cause spasticity via stretch reflex hyperexcitability in the spinal cord, while spastic symptoms, such as involuntary muscle contraction in the hands and fingers, severely restrict skilled hand movements. However, the underlying brain arc mechanisms remain unknown. Here, we demonstrated that neuronal activity increases within the contralesional brainstem nucleus medullary reticular formation (MdV) at the acute post-stroke phase, and the increase in neuronal activity markedly appears by electrostimulation for spasticity induction. Interestingly, ascending electrostimulation signals inhibited the ipsilateral MdV activity. Moreover, in the acute phase with spasticity, the GluA1 density at synapses in MdV neurons was significantly increased, and the ratio of AMPAR subunits transitioned from GluA1 to GluA2 at 2 weeks post-stroke. Thus, this homeostatic plasticity is a mechanism of spasticity. These results provide new insights into the relationship between impaired skilled movements and spasticity symptoms at the acute post-stroke phase.