Autism spectrum disorder (ASD) is the fastest-growing
developmental disorder in the United States. According to the Centers for Disease Control,
one in 68 children is living with an ASD, with associated costs estimated at
between $12 billion and $61 billion.
ASD can impair empathy, the ability to share and understand the
feelings of others, which is aided by the ability to read facial
expression, tone of voice and other social cues.
‘Empathy-like behavior was induced by researchers by identifying then manipulating a brain circuit in an experimental model. This suggests that new strategies may help people with autism spectrum disorder gain social abilities.’
There are no approved pharmacological
approaches that target the social impairments in ASD. The development of
new approaches requires a better understanding of the neural changes
that cause the main symptoms of ASD. This study is a major step toward
Researchers at Rosalind Franklin University of Medicine and Science
have induced empathy-like behavior by identifying then manipulating a
brain circuit in an experimental model, an indication that new
strategies may help people with autism spectrum disorder (ASD) gain
led by Chicago Medical School Professor Amiel Rosenkranz, Department of
Cellular and Molecular Pharmacology, sheds light on the specific role
of the amygdala, an often overlooked brain region, in social behavior
and its pathology in autism.
Published in the journal Nature Neuroscience
findings change the conceptualization of the brain regions important in
empathy and provide the rationale to target the amygdala in certain
forms of ASD.
Investigators measured the empathy-like responses of a rodent while
witnessing an "actor" rodent respond to a mild "startle." The "witness"
quickly developed behaviors that matched the startled subject,
reflecting a behavior that is a foundation for empathy. In addition, the
witness learned that the emotional cues produced by the actor indicate
that something in the environment may be dangerous.
However, when parts
of the amygdala were shut down, the witness did not show empathy-like
responses toward the other. Specifically, the medial amygdala was
required for the witness to display empathy, while a circuit from the
lateral nucleus of the amygdala to the medial (LA-MeA) was required to
learn that the behavior of the actor signaled danger in the environment.
To gain insight into the relevance of these findings for ASD, the
study then examined impaired empathy caused by experimental deletion of
Nrxn1, an analog of a human autism-associated gene (NRXN). Deletion of
Nrxn1 was associated with a lack of empathy-like behavior in the
witness, which investigators found to be correlated with poor neuronal
function in the LA-MeA circuit.
Switching on the LA-MeA circuit in the
non-empathic witness led to the emergence of empathic behaviors. The
findings identify a specific anatomy in the amygdala that may underlie
empathy and demonstrate a particular pathology in the amygdala that may
induce social difficulties caused by autism-related mutations.