Recognition and diagnosis of autism spectrum disorders (ASDs) is increasing across the world. However, effective models for how and why ASD develops are unavailable due to the complexity of the brain and the lack of understanding of its fundamental processes during development.
One common symptom of ASD is aggressive behavior. Understanding this, as the authors say, will help to develop better treatments. Using mice who have an accepted ASD phenotype (they demonstrate autistic-like behaviors that are useful for studying the underlying causes of autism), the authors looked at differences in the amygdala, an area known to modulate aggressive behavior in both mice and humans.
Here is the full scientific article if you wish to download it.
The effects of cannabinoid type 1 receptor (CB1 Receptor) agonists (drugs that bind to the receptors) on the amygdala were observed in these aggressive mice. When the CB1R agonists were administered, there were significant differences in behavior and the action of the basolateral amygdala. This suggests that this could be an avenue for further investigation.
Nearly 40 percent of diagnosed ASD individuals exhibit aggressive behaviors. This is not just distressing to those suffering from autism, it can severely limit their access to education, social interaction, jobs, and healthcare. Aggressive behavior is also commonly accompanied by self-harming behavior, leading to a high prevalence of institutionalization. Clearly, if the reasons for this behavior can be identified, treatments could be developed.
Aggressive Behavior Is Related to Differences in the Amygdala
Recent data have shown that “changes in neural activity within the amygdala and connectivity between the amygdala and other brain regions” can lead to aggressive behaviors. In this study, one protein that is very important to synaptic transmission (how neurons communicate) in this area of the brain were altered to see if it had any effect.
This study used CB1R agonists to alter the signaling in one area of autistic-like mice basolateral amygdalas. The overall effect of CB1R agonists (such as THC) was a reduction in aggressive behavior, which is already a promising result. However, the authors investigated how this effect might have been attained.
In the basolateral amygdala, the synaptic activity was altered, changing how it communicated with itself and the rest of the brain. To be precise, “decreased inhibitory postsynaptic activity alongside an increase in excitatory post-synaptic activity”. Decreased inhibition and increased excitation of these crucial aggression modulating circuits is apparently part of the reason for the different behaviors observed.
The role of CB1R in basolateral amygdala aggression modulation is clearly important. Can mutations like the ones exploited in this study be identified in humans? Can aggression in humans with ASD be treated with CB1R agonists? What are the mechanisms that produce this effect? Could targeting this area of the brain during development prevent aggressive behaviors from developing? Additionally, what is the role of CBD in autism, as it also affects binding to CB1R.
This study has very helpfully identified the role of CB1R in aggressive behavior in autistic-like mice. Whether this is true in humans, who have more complex brains, is not known. CB1R agonists are potentially useful for reducing aggression in ASD individuals.