Common medication restores social deficits in autism mouse model
In the study, first authors Dr. Hannah Schoch and Dr. Arati Kreibich, both of the University of Pennsylvania, and colleagues found that neurons in the amygdala of mice lacking one copy of Pcdh10 (Pcdh10+/-) had reduced levels of NMDA glutamate receptor subunits, indicating disrupted excitatory neural circuitry. "Our study of Pcdh10+/- mice gives us greater insight into the biology of social behaviors and into the function of a gene associated with ASD," said senior author Professor Edward Brodkin, also of the University of Pennsylvania. The study also suggests a possible target for treatment of ASD. When the researchers gave the mice a medication called d-cycloserine, the impaired social behavior improved. D-cycloserine is an old medication that was developed as a treatment for tuberculosis. However, nearly 30 years ago, it was discovered that this drug targets the NMDA glutamate receptor to enhance its function. Brodkin cautions that although much more work would b...