Experiments in zebrafish reveal a new role for a critical hypothalamic transcription factor, orthopedia, in controlling developmental neuropeptide balance in a discrete oxytocin-producing neuronal circuit whose disrupted development affects social behavior.
Changes in Shank gene dosage alter voltage-activated calcium current and calcium-activated gene expression in a manner that parallels the effects of human Shank copy number variation on psychiatric disease risk.
The subjective time of social interactions reflects one's autistic-like tendency and is critically mediated by oxytocin, indicating that time perception is ingrained with personality traits, which likely have neuroendocrine origins as per previous research.
Mirroring human patients with ARID1B mutations, Arid1b haploinsufficient mice exhibited numerous neuropsychiatric defects and revealed IGF1 deficiency related growth impairment that could be ameliorated with growth hormone supplementation.
Electrophysiological recordings reveal domains within the extracellular and intracellular region of neuroligin important for specifying and carrying out its function at inhibitory synapses respectively.
Social-interaction impairment in germ-free mice is associated with a markedly altered transcriptional response to social novelty in the amygdala, as characterised by replacement of upregulation of common stimulus-induced pathways with upregulation of the splicing machinery.
Mice that lack the autism susceptibility gene Semaphorin 5A show excess excitatory synapse formation in dentate granule neurons and also altered social behavior, adding to evidence that a surplus of synapses contributes to the behavioral changes observed in autism spectrum disorders.
Publication bias, in which positive results are preferentially reported by authors and published by journals, can restrict the visibility of evidence against false claims and allow such claims to be canonized inappropriately as facts.