Evading threats relies on deploying complex avoidance strategies such as deciding between escape and motor arrest. Although studies across vertebrates indicate that the brainstem is critical for motor arrest, the mechanisms remain elusive. A recent study in zebrafish showed that upon sensory-motor mismatch, passivity involves noradrenergic signaling eliciting a brain-wide glial calcium wave. However, it remains unknown how noradrenergic activation translates into subsequent glial calcium waves and provokes motor arrest. Our working hypothesis is that noradrenergic neurons integrate intensive sensory stimulations and control the decision and duration of motor arrest. Exploiting the transparency and genetic accessibility of larval zebrafish, we found that upon graded optogenetic activation of noradrenergic neurons, short activation (<1s) didn't induce motor arrest, while long durations (>1s) induced prolonged motor arrest whose durations scaled with the duration of noradrenergic activation. These results suggest sustained activation of noradrenergic neurons is required for the animal to employ motor arrest. To decipher the nature of the glial calcium wave associated with motor arrest, we monitored the activity of glial cells upon activating noradrenergic neurons. Short activations elicited a synchronous, small calcium rise confined to glia in the spinal cord, while long activations elicited a large glial wave that started in the rostral spinal cord and propagated to the brainstem, invading the obex, pons, and medulla. These findings indicate that sustained noradrenergic activation is necessary to induce a glial calcium wave that reaches the brainstem to elicit motor arrest. Further work will investigate the mechanisms underlying the blockade of motor output.