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Researchers induce social deficits associated with autism, schizophrenia in mice

Researchers induce social deficits associated with autism, schizophrenia in mice

Stanford researchers, led by practicing psychiatrist Karl Deisseroth, MD, PhD, have successfully induced behavioral symptoms of autism and schizophrenia in mice. Their findings were published today in Nature.

Researchers used optogenetics, a Stanford-developed method allowing for precise manipulation of activity in the brain, to elevate certain nerve circuits’ susceptibility to stimulation. They discovered that this increase in susceptibility triggered the kind of abnormal social behavior in the mice that is associated with diseases like autism and schizophrenia in humans.

Multiple hypotheses exist to explain why increased sensitivity to stimulation would lead to the kind of social abnormalities that autistic and schizophrenic patients experience. One hypothesis holds that in these humans’ brains, excitatory and inhibitory nerve cells exhibit an altered tendency to fire, which could result in hyper-responsiveness to stimulation. This is consistent with autistic behavior, explains the release:

In addition, said Deisseroth, “autistic kids seem to be over-responding to environmental stimuli.” For instance, they find eye contact overwhelming, or may cover their ears if there are too many people talking at once.

These findings are particularly important given that no medications currently exist to treat the social-behavioral symptoms of either disorder.

Previously: Stanford expert discusses environmental and genetic factors in autism risk and Using light to better understand mental illness

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