Hedgehog signaling is necessary and sufficient to mediate craniofacial plasticity in teleosts.

Phenotypic plasticity, the ability of a single genotype to produce multiple phenotypes under different environmental conditions, is critical for the origins and maintenance of biodiversity; however, the genetic mechanisms underlying plasticity as well as how variation in those mechanisms can drive evolutionary change remain poorly understood. Here, we examine the cichlid feeding apparatus, an icon of both prodigious evolutionary divergence and adaptive phenotypic plasticity. We first provide a tissue-level mechanism for plasticity in craniofacial shape by measuring rates of bone deposition within functionally salient elements of the feeding apparatus in fishes forced to employ alternate foraging modes. We show that levels and patterns of phenotypic plasticity are distinct among closely related cichlid species, underscoring the evolutionary potential of this trait. Next, we demonstrate that hedgehog (Hh) signaling, which has been implicated in the evolutionary divergence of cichlid feeding architecture, is associated with environmentally induced rates of bone deposition. Finally, to demonstrate that Hh levels are the cause of the plastic response and not simply the consequence of producing more bone, we use transgenic zebrafish in which Hh levels could be experimentally manipulated under different foraging conditions. Notably, we find that the ability to modulate bone deposition rates in different environments is dampened when Hh levels are reduced, whereas the sensitivity of bone deposition to different mechanical demands increases with elevated Hh levels. These data advance a mechanistic understanding of phenotypic plasticity in the teleost feeding apparatus and in doing so contribute key insights into the origins of adaptive morphological radiations.

The role of imitation in the observed heterogeneity in EEG mu rhythm in autism and typical development.

Dysfunction in an execution/observation matching system, or mirror neuron system, has been proposed to contribute to the social deficits observed in Autism Spectrum Disorder (ASD). Atypical activity in this system, as reflected in attenuation of the EEG mu rhythm, has been demonstrated in several studies; however, normative patterns of activity have been evident in other ASD samples. The current study sought to investigate this poorly understood heterogeneity in social perceptual brain function in ASD. EEG mu rhythm was recorded in a well-characterized sample of 19 children with ASD (mean age=6.4; 1 female) and 19 age-matched typically developing peers (mean age=6.9; 2 females) during execution and observation of goal-directed hand actions. Children were assessed on variables theoretically related to mirror neuron system function (MNS), such as ASD symptoms and imitation ability. Results indicated that MNS activity was associated with facial imitation ability, but not hand imitation ability, in children with ASD and typically developing individuals. Groups were comparable in terms of average MNS activity during both action observation and execution, but, in both groups, a subset of children showed absent or significantly reduced MNS activity during observation of action in conjunction with greater difficulty in imitation. These results emphasize the relationship between EEG indices of MNS function and imitative skill and suggest that dysfunction of the MNS is related to imitation ability in both clinical and typical populations, rather than representing a core deficit or universal impairment in ASD.

The Early Start Denver Model Intervention and Mu Rhythm Attenuation in Autism Spectrum Disorders.

We examined the relationship between the Early start Denver model (ESDM) intervention and mu rhythm attenuation, an EEG paradigm reflecting neural processes associated with action perception and social information processing. Children were assigned to either receive comprehensive ESDM intervention for two years, or were encouraged to pursue resources in the community. Two years after intervention, EEG was collected during the execution and observation of grasping actions performed by familiar and unfamiliar agents. The ESDM group showed significantly greater attenuation when viewing a parent or caregiver executing a grasping action, compared with an unfamiliar individual executing the same action. Our findings suggest that the ESDM may have a unique impact on neural circuitry underlying social cognition and familiarity.

Modeling temporal dynamics of face processing in youth and adults.

A hierarchical model of temporal dynamics was examined in adults (n = 34) and youth (n = 46) across the stages of face processing during the perception of static and dynamic faces. Three ERP components (P100, N170, N250) and spectral power in the mu range were extracted, corresponding to cognitive stages of face processing: low-level vision processing, structural encoding, higher-order processing, and action understanding. Youth and adults exhibited similar yet distinct patterns of hierarchical temporal dynamics such that earlier cognitive stages predicted later stages, directly and indirectly. However, latent factors indicated unique profiles related to behavioral performance for adults and youth and age as a continuous factor. The application of path analysis to electrophysiological data can yield novel insights into the cortical dynamics of social information processing.

Modulation of mu attenuation to social stimuli in children and adults with 16p11.2 deletions and duplications.

BACKGROUND: Copy number variations (CNV) within the recurrent ~600 kb chromosomal locus of 16p11.2 are associated with a wide range of neurodevelopmental disorders, including autism spectrum disorder (ASD). However, little is known about the social brain phenotype of 16p11.2 CNV and how this phenotype is related to the social impairments associated with CNVs at this locus. The aim of this preliminary study was to use molecular subtyping to establish the social brain phenotype of individuals with 16p11.2 CNV and how these patterns relate to typical development and ASD. METHODS: We evaluated the social brain phenotype as expressed by mu attenuation in 48 children and adults characterized as duplication carriers (n = 12), deletion carriers (n = 12), individuals with idiopathic ASD (n = 8), and neurotypical controls (n = 16). Participants watched videos containing social and nonsocial motion during electroencephalogram (EEG) acquisition. RESULTS: Overall, only the typical group exhibited predicted patterns of mu modulation to social information (e.g., greater mu attenuation for social than nonsocial motion). Both 16p11.2 CNV groups exhibited more mu attenuation for nonsocial than social motion. The ASD group did not discriminate between conditions and demonstrated less mu attenuation compared to the typical and duplication carriers. Single-trial analysis indicated that mu attenuation decreased over time more rapidly for 16p11.2 CNV groups than the typical group. The duplication group did not diverge from typical patterns of mu attenuation until after initial exposure. CONCLUSIONS: These results indicate atypical but unique patterns of mu attenuation for deletion and duplication carriers, highlighting the need to continue characterizing the social brain phenotype associated with 16p11.2 CNVs.

EEG mu rhythm in typical and atypical development.

Electroencephalography (EEG) is an effective, efficient, and noninvasive method of assessing and recording brain activity. Given the excellent temporal resolution, EEG can be used to examine the neural response related to specific behaviors, states, or external stimuli. An example of this utility is the assessment of the mirror neuron system (MNS) in humans through the examination of the EEG mu rhythm. The EEG mu rhythm, oscillatory activity in the 8-12 Hz frequency range recorded from centrally located electrodes, is suppressed when an individual executes, or simply observes, goal directed actions. As such, it has been proposed to reflect activity of the MNS. It has been theorized that dysfunction in the mirror neuron system (MNS) plays a contributing role in the social deficits of autism spectrum disorder (ASD). The MNS can then be noninvasively examined in clinical populations by using EEG mu rhythm attenuation as an index for its activity. The described protocol provides an avenue to examine social cognitive functions theoretically linked to the MNS in individuals with typical and atypical development, such as ASD.