| First Author | Zhang K | Year | 2014 |
| Journal | Neuroscience | Volume | 275 |
| Pages | 238-47 | PubMed ID | 24952328 |
| Mgi Jnum | J:215394 | Mgi Id | MGI:5605217 |
| Doi | 10.1016/j.neuroscience.2014.06.020 | Citation | Zhang K, et al. (2014) Loss of glutamic acid decarboxylase (Gad67) in Gpr88-expressing neurons induces learning and social behavior deficits in mice. Neuroscience 275:238-47 |
| abstractText | GABA is the neurotransmitter of striatal projection neurons, however the contribution of the striatal GABAergic output to behavior is not well understood. We assessed motor function, spatial learning, social behavior, olfactory and object recognition preferences in mice lacking the GABA-synthesizing enzyme glutamic acid decarboxylase, Gad67, in neurons expressing the protein Gpr88, an orphan G-protein-coupled receptor primarily expressed in the striatum. Gad67-deficient mice show no impairments in motor coordination and balance, but exhibit enhanced locomotor activity and stereotypic grooming behavior. Furthermore, Gad67-deficient mice show impairments in spatial learning, social behavior, olfactory preferences, and they prefer a familiar compared to a novel object in the object recognition test. These findings provide original evidence that striatal Gad67 expression is involved in the modulation of learning and social behavior. Some of the behavioral abnormalities observed in Gad67-deficient mice are reminiscent of Autism-spectrum-disorder (ASD) deficits, suggesting that abnormal striatal GABAergic output may contribute to behavioral deficits in ASD. |
