Self-injurious behavior is a debilitating characteristic that is highly prevalent in autism spectrum disorders. Afflicted children bang their heads, punch or slap their faces, and bite at their hands and arms. These behaviors carry the risk of severe physical injury, and they interfere with all normal educational and social activities. In addition, self-injury is extremely disruptive to families of autistic children, and the annual cost for specialized treatment is staggering. Our current knowledge of the genetic and biochemical basis of autism spectrum disorders does not reveal the reasons why autistic children are vulnerable to develop self-injury (over one-third of autistic children self-injure). However, evidence from human and animal studies suggests that defects in the functioning of two brain chemicals (dopamine and glutamate) may underlie the development of self-injury.
We have developed and refined an animal model of self-injurious behavior, and we are using this model to study the contributions of defective dopamine and glutamate function. In our model, rats will start to exhibit self-biting behavior after 4 to 6 days of treatment with a drug (known as pemoline) that increases dopamine function, and we can prevent the induction of this self-injury using a drug (known as MK-801) that diminishes glutamate function. These data further support the putative roles of dopamine and glutamate in self-injury. We are now studying biochemical changes in the brains of self-injurious rats when we administer pemoline and comparing the brains of these rats with the brains of rats that receive pemoline plus MK-801 and do not self-injure.