To cerebellar tonsil
Scientists have rebalanced the brain: a mechanism now discovered may represent a general principle of emotional regulation.
A team of researchers has just discovered a specific set of neurons in amygdala – brain region associated with the processing of emotions – whose hyperactivity can cause anxiety, depression and social deficits.
The study led by Juan Lerma, in the journal iScience, demonstrates that restoring the balance of neuronal excitability in a specific area of the amygdala is enough to reverse these behaviors — at least, in laboratory rats.
Scientists already knew that the amygdala plays a central role in fear and anxiety responses, but this research identified a neuronal population whose unbalanced activityin itself, is capable of causing pathological behaviors.
The team used genetically modified mice with overexpression of the gene Greece4responsible for increasing the production of GluK4-type glutamate receptors and, consequently, neuronal excitability. These animals showed symptoms similar to those seen in people with disorders such as autism or schizophrenia.
By normalizing gene expression in neurons located in the basolateral amygdala, the researchers were able to reestablish communication with a group of inhibitory neurons in the centrolateral amygdala. This simple correction was enough to reverse anxiety and social deficit behaviors.
The team evaluated the animals through electrophysiological recordings and behavioral tests that measure anxiety, depression and social interaction, including experiments that analyze preference for open or closed spaces and interest in other individuals. Using genetic engineering tools and modified viruses, scientists were able to precisely correct neuronal dysfunction and observe corresponding changes in behavior.
The same method was then applied to unmodified mice that had naturally higher levels of anxiety. The treatment also reduced these levels, reinforcing the idea that the discovered mechanism may represent a general principle of emotional regulation in the brain.
Although some cognitive deficiencies, such as failures in object recognition memory, were not corrected — suggesting the involvement of other regions such as the hippocampus — the results open new therapeutic perspectives.
