| First Author | Fendt M | Year | 2010 |
| Journal | Genes Brain Behav | Volume | 9 |
| Issue | 1 | Pages | 33-44 |
| PubMed ID | 19740090 | Mgi Jnum | J:169208 |
| Mgi Id | MGI:4940009 | Doi | 10.1111/j.1601-183X.2009.00532.x |
| Citation | Fendt M, et al. (2010) The effect of mGlu8 deficiency in animal models of psychiatric diseases. Genes Brain Behav 9(1):33-44 |
| abstractText | 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. |
