Abstract
The brain includes multiple types of interconnected excitatory and inhibitory neurons that together allow us to move, think, feel, and interact with the environment. Inhibitory interneurons (INs) comprise a small, heterogeneous fraction, but they exert a powerful and tight control over neuronal activity and consequently modulate the magnitude of neuronal output and, ultimately, information processing. IN abnormalities are linked to two pediatric psychiatric disorders with high comorbidity: autism spectrum disorder (ASD) and Tourette syndrome (TS). Studies probing the basis of this link have been contradictory regarding whether the causative mechanism is a reduction in number, dysfunction, or gene aberrant expression (or a combination thereof). Here, we integrate different theories into a more comprehensive view of INs as responsible for the symptomatology observed in these disorders. IN dysfunction in corticostriatal circuits leads to TS and ASD. Differences in the location of these abnormalities could be the key that can lead to either TS or ASD. Reduced GABAergic tone in both disorders generates an excitatory/inhibitory imbalance that produces the core behaviors in both disorders. There is strong evidence for a critical role of the striatum in TS, but only recently have a series of studies demonstrated a new hypothesis of the striatum as a key participant in ASD.
| Original language | English |
|---|---|
| Pages (from-to) | 397-407 |
| Number of pages | 11 |
| Journal | Trends in Neurosciences |
| Volume | 40 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jul 2017 |
Keywords
- Tourette syndrome
- autism
- cortex
- interneurons
- striatum
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