| First Author | Löw K | Year | 2000 |
| Journal | Science | Volume | 290 |
| Issue | 5489 | Pages | 131-4 |
| PubMed ID | 11021797 | Mgi Jnum | J:65100 |
| Mgi Id | MGI:1891777 | Doi | 10.1126/science.290.5489.131 |
| Citation | Low K, et al. (2000) Molecular and neuronal substrate for the selective attenuation of anxiety. Science 290(5489):131-4 |
| abstractText | Benzodiazepine tranquilizers are used in the treatment of anxiety disorders. To identify the molecular and neuronal target mediating the anxiolytic action of benzodiazepines, we generated and analyzed two mouse lines in which the alpha2 or alpha3 GABA(A) (gamma-aminobutyric acid type A) receptors, respectively, were rendered insensitive to diazepam by a knock-in point mutation. The anxiolytic action of diazepam was absent in mice with the alpha2(H101R) point mutation but present in mice with the alpha3(H126R) point mutation. These findings indicate that the anxiolytic effect of benzodiazepine drugs is mediated by alpha2 GABA(A) receptors, which are largely expressed in the limbic system, but not by alpha3 GABA(A) receptors, which predominate in the reticular activating system. |
