Vikaas Sohal and John Rubenstein found that Pogz heterozygous mice exhibited reduced anxiety-related avoidance behavior and that this correlated with impaired communication between the ventral hippocampus and medial prefrontal cortex.
Research Highlights
Highlights of SFARI-funded papers, selected by the SFARI science team.
Vanessa Troiani and colleagues demonstrated a linear relationship between pupil dilation, reward/punishment sensitivity and individual ASD diagnostic status.
Cellular system to screen ASD risk gene function
Robi Mitra and colleagues have developed a scalable CRISPR/Cas9 RNA sequencing assay in a human neuronal differentiation cell model, enabling high-throughput assessments of how repression of ASD risk genes affects transcription and neuronal differentiation.
Mitochondrial deficiency and fragile X syndrome
Elizabeth Jonas and colleagues identified a molecular mechanism underlying the contributions of mitochondrial dysfunction to the synaptic and behavioral features associated with fragile X syndrome.
Neural circuitry of sociability in mice
Hirofumi Morishita and colleagues showed that juvenile social isolation leads to deficits in adult mouse sociability via reduced activation of a prefrontal-paraventricular thalamus circuit.
Sex differential effects of excitation-inhibition imbalance in autism
Stefano Panzeri and colleagues used neuroimaging-derived measures to assess the sex differential impact of excitation/inhibition imbalance in idiopathic ASD.
ASD risk genes and homeostatic plasticity
Graeme Davis and colleagues showed that ASD risk genes genetically interact with a class of common modifiers of presynaptic homeostatic plasticity at the Drosophila neuromuscular junction.
Parental influence on language development in infants at high and low risk for autism
Charles Nelson, Helen Tager-Flusberg and colleagues assessed language development in infants at high risk and low risk of ASD. They reported parental mean length of utterance as a possible difference in the high-risk group.
Mutations in ACTL6B are linked to a form of recessive autism
Gerald Crabtree, Joseph Gleeson and colleagues defined a new recessive form of ASD caused by mutations in ACTL6B, part of the BAF complex, which regulates activity-responsive transcription in resting neurons.
MeCP2 and VIP-interneurons
Jessica Cardin and colleagues identified an important and unexpected role for the VIP subclass of interneurons in mediating the functions of MeCP2 in the development of cortical circuits.
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