Pharmacological animal models of Tourette syndrome

Maya Bronfeld, Michal Israelashvili, Izhar Bar-Gad

Research output: Contribution to journalReview articlepeer-review

44 Scopus citations

Abstract

Pharmacological animal models of Tourette syndrome (TS) are an important tool for studying the neural mechanisms underlying this disorder. Dysfunction of the cortico-basal ganglia (CBG) system has been widely implicated in TS but the exact nature of this dysfunction is unknown. Pharmacological treatments of TS have prompted multiple hypotheses regarding the involvement of different neuromodulators in the disorder. Pharmacological manipulations in animal models were used to investigate the relationships between these neuromodulators and different symptoms of TS, including motor (tics) and non-motor (sensorimotor gating deficits) phenomena. Models initially focused on the direct effects of pharmacology on behavior, and only recently have begun providing neurophysiological data reflecting the neuronal mechanism linking the two. Animal models support the notion of CBG dysfunction as the neural mechanism underlying TS, and suggest that it may be derived from either direct deficits of local striatal GABAergic networks or a dysfunction of the neuromodulator systems controlling them. These findings can provide the much- needed conceptual construct for the TS etiology and point to new therapeutic targets.

Original languageEnglish
Pages (from-to)1101-1119
Number of pages19
JournalNeuroscience and Biobehavioral Reviews
Volume37
Issue number6
DOIs
StatePublished - Jul 2013

Bibliographical note

Funding Information:
This work was supported by Israel Science Foundation (ISF) grant 327/09 and a Tourette Syndrome Association (TSA) grant.

Keywords

  • Animal models
  • Basal ganglia
  • Dopamine
  • GABA
  • Limbic system
  • Motor system
  • Motor tics
  • Pharmacology
  • Primate
  • Rat
  • Sensorimotor gating
  • Stereotypic behavior
  • Striatum
  • Tourette syndrome

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