Some social issues in DYRK1A model mice stem from faulty inhibitory circuits
Alterations in inhibitory circuits and difficulties in social recognition characterize mice missing one copy of DYRK1A, a gene linked to autism.
Alterations in inhibitory circuits and difficulties in social recognition characterize mice missing one copy of DYRK1A, a gene linked to autism.
Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.
Neurons with a faulty copy of SETD1A, a gene tied to autism and schizophrenia, show structural abnormalities and altered connectivity patterns.
The animals recall fear more readily if a set of inhibitory neurons in the hippocampus is switched on.
The protein, FMRP, shapes cell signaling near synapses but switches to regulate genes in the cell body, according to new research.
Mice that express a fluorescent synaptic receptor reveal the interactions between neurons in unprecedented detail.
Deleting a copy of the gene TBX1 depletes the fatty myelin insulation that surrounds neurons and reduces cognitive speed in mice.
Jolting a bundle of nerve fibers deep in the brain restores learning and memory in mice with mutations of the autism-linked gene CDKL5.
Researchers are increasingly turning to simple animals to learn about autism biology and find leads for new drugs.
Neurons in mice with an autism-linked mutation sprout extraneous protrusions, an overgrowth accompanied by above-average motor learning. Inhibiting a cell signaling pathway reverses the effect.