Noradrenaline (NA) is a strong modulator of neuronal activity and many autism spectrum disorder (ASD) symptoms can be attributed to maladaptive activity of locus coeruleus (LC), the main source of forebrain NA. Our lab recently uncovered a role for dysregulated LC-NA function in motor learning delays of the 16p11.2 deletion (+/-) mouse-model of ASD. We found that reduced NA levels in primary motor cortex (M1) caused delays in motor learning and increased neuronal activity in M1 pyramidal neurons. Both behavioral and neuronal phenotypes were rescued by chemogenetic activation of LC-NA. We next aimed to fully characterize the M1 NA dynamics at different learning stages. I employed a newly developed optical NA-sensor, GRABNE, with in vivo two-photon imaging to visualize spatiotemporal release patterns of NA in M1 throughout a motor learning task. Intriguingly, wild-type exhibited consistently elevated NA levels during behavior, while 16p11.2+/- exhibited a delay in behaviorally induced NA increases. In addition to the delay in temporal dynamics, 16p11.2+/- showed altered spatial dynamics, with sparser and less behavior-specific NA release across M1 during early learning stages. This work provides a novel glimpse into LC-NA dysfunction in ASD, permitting an improved understanding of the role for NA in modulation and behavior.