Somatosensory Regions Show Limited Functional Connectivity Differences in Youth with Autism Spectrum Disorder.

An estimated 70-90% of children with autism spectrum disorder (ASD) have sensory symptoms, which may present as hyper- or hyporesponsivity in one or more sensory modalities. These sensitivities correlate with social symptoms, activity, and social interaction levels. Interestingly, sensory symptoms appear to be most prevalent in late childhood, suggesting a developmental component. Although the neural basis of sensory sensitivities remains unclear, atypical functional connectivity of sensory brain regions has been suggested as a potential mechanism. Tactile sensitivities are among the most predictive of social functioning, yet no studies to our knowledge have examined somatosensory functional connectivity in children and adolescents with ASD, when symptoms are typically most prominent. In this study, we used human data from the Autism Brain Imaging Data Exchange (ABIDE-I) to assess functional connectivity differences of somatosensory regions during resting state functional magnetic resonance imaging, in youth aged 8-15 years. After head motion exclusion, our sample included 67 participants with ASD and 121 typically developing controls. We additionally examined associations between functional connectivity and age, as well as ASD symptom severity. Together, these seed-based analyses showed limited differences in functional connectivity between groups, either to hypothesized target regions or in terms of global connectivity. Our findings suggest that hyper- or hyposomatosensory functional connectivity at rest is not a population-level feature in ASD. However, this does not preclude increased variability of somatosensory networks across the ASD population. Furthermore, as sensory sensitivities were not specifically assessed in this sample, future studies may be better able to identify patterns of functional connectivity, reflecting individual differences in sensory symptoms.

Pharmacological induction of skin pigmentation unveils the neuroendocrine circuit regulated by light.

Light-regulated skin colour change is an important physiological process in invertebrates and lower vertebrates, and includes daily circadian variation and camouflage (i.e. background adaptation). The photoactivation of melanopsin-expressing retinal ganglion cells (mRGCs) in the eye initiates an uncharacterized neuroendocrine circuit that regulates melanin dispersion/aggregation through the secretion of alpha-melanocyte-stimulating hormone (α-MSH). We developed experimental models of normal or enucleated Xenopus embryos, as well as in situ cultures of skin of isolated dorsal head and tails, to analyse pharmacological induction of skin pigmentation and α-MSH synthesis. Both processes are triggered by a melanopsin inhibitor, AA92593, as well as chloride channel modulators. The AA9253 effect is eye-dependent, while functional data in vivo point to GABAA receptors expressed on pituitary melanotrope cells as the chloride channel blocker target. Based on the pharmacological data, we suggest a neuroendocrine circuit linking mRGCs with α-MSH secretion, which is used normally during background adaptation.