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Generating Acute and Chronic Experimental Models of Motor Tic Expression in Rats
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Common neuronal mechanisms underlying tics and hyperactivity.

Michal Israelashvili1, Dorin Yael1, Esther Vinner1

  • 1The Leslie & Susan Goldschmied (Gonda) Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat-Gan, Israel.

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|April 4, 2020
PubMed
Summary
This summary is machine-generated.

Tourette syndrome (TS) and attention deficit hyperactivity disorder (ADHD) share common striatal disinhibition mechanisms. These neuronal changes manifest differently, causing distinct motor tics or hyperactivity symptoms.

Keywords:
Animal modelAttention deficit hyperactivity disorder (ADHD)Basal gangliaNeurophysiologyTourette syndrome

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Area of Science:

  • Neuroscience
  • Neurobiology
  • Behavioral Science

Background:

  • Tourette syndrome (TS) and attention deficit hyperactivity disorder (ADHD) are highly comorbid neurodevelopmental disorders.
  • The underlying neuronal mechanisms and sources of comorbidity remain largely unknown.

Purpose of the Study:

  • To investigate the similar and distinct neuronal components underlying Tourette syndrome-like and ADHD-like symptoms.
  • To explore the role of striatal disinhibition in the expression of these disorders.

Main Methods:

  • Examined neuronal activity in freely behaving rats before and after focal striatal disinhibition.
  • Injected substances into different functional domains of the striatum (motor and limbic).
  • Recorded macro-scale and micro-scale neuronal changes and correlated them with behavioral outcomes.

Main Results:

  • Focal striatal disinhibition induced motor tics (motor domain) or hyperactivity (limbic domain).
  • Disinhibition caused similar neuronal changes across striatal locations, but with domain-specific behavioral outcomes.
  • Hyperactivity appeared linked to limbic domain changes without direct motor domain activation.

Conclusions:

  • Tic expression and hyperactivity share common local neuronal activity changes within the striatum.
  • These shared neuronal changes result in distinct behavioral and neuronal outcomes, suggesting a link between TS and ADHD.
  • Striatal disinhibition, potentially due to GABAergic alterations, may be a common mechanism for hyper-behavioral disorders.