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.
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.
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.