Computerized three-dimensional modeling shows nerve cell abnormalities in the hippocampus of fragile X mice — and suggests the importance of raising experimental mice in more natural habitats, according to a poster presented Wednesday at the Society for Neuroscience annual meeting in San Diego.

The brains of young mice with fragile X syndrome show a dearth of two proteins that are important at the synapse, the junction between neurons, researchers reported Tuesday at the Society for Neuroscience annual meeting in San Diego.

The Allen Institute for Brain Science has released whole-genome expression data from one-and-a-half adult human brains, and is gathering information from samples at different stages of development, from four weeks after conception to adulthood. The data were described at poster sessions Saturday and Tuesday at the Society for Neuroscience annual meeting in San Diego.

People with autism have structural differences in the temporal cortex — a brain region involved in sound and language processing — compared with controls, according to a postmortem study presented Monday at the Society for Neuroscience annual meeting in San Diego.

The gene-environment interactions that are thought to contribute to many cases of autism can now be explored in a mouse model, according to a poster presented Sunday at the Society for Neuroscience annual meeting in San Diego.

Infection early in pregnancy is more harmful to the fetus than at later stages, triggering brain and behavioral changes in the offspring similar to those seen in people with schizophrenia, according to two mouse studies published in October. A third study suggests that exercise can mitigate some of these effects.

Mice missing a large protein at the junction between neurons show motor impairments, anxiety and increased social behaviors, according to a study in the American Journal of Psychiatry. The protein, postsynaptic density-95 or PSD-95, is part of a key molecular bridge connecting other proteins linked to autism.

The protein missing in fragile X syndrome is necessary for the proper development of neural stem cells — self-renewing cells that can differentiate into more specialized types, including neurons — according to a paper published in the August issue of Human Molecular Genetics.

The amygdala, a brain region that regulates fear and anxiety, shows abnormal neuronal signaling in a mouse model of fragile X syndrome, according to two studies published this summer. These are the first to explore cellular defects in the region in fragile X.

Researchers have uncovered an important molecular piece of a learning mechanism that occurs at the junction between neurons. The findings, which may help understand how the brain is disrupted in disorders such as autism, appear in the 24 June issue of Neuron.