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The effect of mGlu8 deficiency in animal models of psychiatric diseases

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • M. Fendt
  • H. Bürki
  • S. Imobersteg
  • H. van der Putten
  • K. McAllister
  • J. C. Leslie
  • D. Shaw
  • Christian Hölscher
<mark>Journal publication date</mark>02/2010
<mark>Journal</mark>Genes, Brain and Behavior
Issue number1
Number of pages12
Pages (from-to)33-44
Publication StatusPublished
<mark>Original language</mark>English


The metabotropic glutamate receptor subtype 8 (mGlu(8)) is presynaptically located and regulates the release of the transmitter. Dysfunctions of this mechanism are involved in the pathophysiology of different psychiatric disorders. mGlu(8) deficient mice have been previously investigated in a range of studies, but the results are contradictory and there are still many open questions. Therefore, we tested mGlu(8)-deficient animals in different behavioral tasks that are commonly used in neuropsychiatric research. Our results show a robust contextual fear deficit in mGlu(8)-deficient mice. Furthermore, novel object recognition, chlordiazepoxide-facilitated extinction of operant conditioning and the acoustic startle response were attenuated by mGlu(8) deficiency. We found no changes in sensory processing, locomotor activity, prepulse inhibition, phencyclidine-induced changes in locomotion or prepulse inhibition, operant conditioning, conditioned fear to a discrete cue or in animal models of innate fear and post-traumatic stress disorder. We conclude that mGlu(8) might be a potential target for disorders with pathophysiological changes in brain areas where mGlu(8) modulates glutamate and gamma-amino butyric acid (GABA) transmission. Our data especially point to anxiety disorders involving exaggerated contextual fear, such as generalized anxiety disorders, and to conditions with disturbed declarative memory.