Much research has been done into the use of a rat model to show how Borna virus infection,[17][18] exposure to valproic acid in utero,[19] and maternal immune activation[20] may cause autism.
It has been observed that mice lacking the gene for oxytocin exhibit deficits in social interaction, and that it may be possible to develop treatments for autism based on abnormalities in this and other neuropeptides.
However, recent studies have emphasized that the majority of risk factors identified for autism do not directly connect to the oxytocin signaling pathway.
Environmental factors have been studied in animal rodent models and have been seen to influence brain development and play a role in gene expression.
Recent advancements in research on ASD in rodent models illustrate that the interaction between genetic predispositions and environmental exposures.
[25]This link between environmental exposures and distinct neurobiological alterations remains unpredictable largely due to the variability of timing.
[29] Overall, recent studies make a case for infection during pregnancy being an environmental risk factor for neurodevelopmental disorders such as ASD or schizophrenia in rodents.
For example, rodents with this gene exhibit elevated cortical spine densities that are similar to those found in autism as well as decreased social behaviors.
One study found that mutations in the NLGN 3 and 4 genes lead to loss of neuroligin processing to stimulate the formation of synapses which is a feature of autistic spectrum disorders2.
Lastly, many of the abnormalities found in autistic spectrum disorders involve the mTOR signaling pathway, the GABA - containing neurons, and the immune system.
In addition, this supports the need for animal models that establish a greater understanding of what effects these particular brain regions and genetics have on development, and if there are measures we can take to prevent the onset of the disorder3.
When exposed to prenatal valproate (VPA) during pregnancy, the mice are born with basic deformities and the developmental delays seen symptomatically in humans5.
During development there are specific times, called critical periods, where the brain is more capable of acquiring neural connections which usually leads to new behavioral and psychological skills.
[30] These parallels extend to the FOXP2 gene, expressed significantly in various parts of CNS, including areas crucial for motor functions, from embryonic development through adulthood.
[31] Other research using this model has been done by Stephanie White at the University of California Los Angeles, who studied mutations in the FOXP2 gene and its potential role in learned vocalization in both songbirds (specifically the zebra finch) and humans.