We examined how correlated firing controls axon remodeling, using in vivo time-lapse imaging and electrophysiological analysis of individual retinal ganglion cell (RGC) axons that were visually stimulated either synchronously or asynchronously relative to neighboring inputs in the Xenopus laevis optic tectum. RGCs stimulated out of synchrony rapidly lost the ability to drive tectal postsynaptic partners while their axons grew and added many new branches. In contrast, synchronously activated RGCs produced fewer new branches, but these were more stable. The effects of synchronous activation were prevented by the inhibition of neurotransmitter release and N-methyl-D-aspartate receptor (NMDAR) blockade, which is consistent with a role for synaptic NMDAR activation in the stabilization of axonal branches and suppression of further exploratory branch addition.

Alexithymia is a personality construct characterized by altered emotional awareness which has been gaining diagnostic prevalence in a range of neuropsychiatric disorders, with notably high rates of overlap with autism spectrum disorder (ASD). However, the nature of its role in ASD symptomatology remains elusive. Here, we distill research at the intersection of alexithymia and ASD. After a brief synopsis of the studies that played a pioneering role in the identification of the overlapping fields between alexithymia and ASD, we comb the literature for evidence of its overlap with ASD in terms of prevalence, etiology, and behaviors. Through a formalized framework of the process of emotional interpretation and expression, we explore evidence for where and how deficits arise in this complex network of events. We portray how these relate to the dynamic interplay between alexithymic and autistic traits and find emerging evidence that alexithymia is both a cause and consequence of autistic behaviors. We end with a strategic proposal for future research and interventions to dampen the impacts of alexithymia in ASD.