| First Author | An JJ | Year | 2004 |
| Journal | Mol Cell Neurosci | Volume | 25 |
| Issue | 4 | Pages | 732-41 |
| PubMed ID | 15080900 | Mgi Jnum | J:91838 |
| Mgi Id | MGI:3050921 | Doi | 10.1016/j.mcn.2003.12.010 |
| Citation | An JJ, et al. (2004) Altered GABAergic neurotransmission in mice lacking dopamine D2 receptors. Mol Cell Neurosci 25(4):732-41 |
| abstractText | The levels of glutamic acid decarboxylase (GAD) were strongly increased in the cortex and the striatum in dopamine D2 receptors null (D2R-/-) mice, which show a significant locomotor impairment. In this study, the effects of different GABAergic drugs on locomotor activity were analyzed in D2R-/- mice. After administering muscimol (1 mg/kg), a GABA(A) receptor agonist, the D2R-/- mice showed increased locomotor activity up to 200%. When the muscimol dose was increased (4-6 mg/kg), the D2R-/- mice exhibited seizure-like behavior, and the electroencephalographic (EEG) recordings during these behaviors showed a high amplitude rhythmic epileptiform activity in these mice. In situ hybridization showed that after injecting muscimol in the D2R-/- mice, the expression of enkephalin and immediate early gene, NGFI-A, was closely regulated with the locomotor activity regulated by GABAergic stimulation. These results suggest that the absence of D2R alters the GABAergic neurotransmission, specifically on GABA(A)-receptor mediated signaling, and stimulating the GABA(A) receptor can reverse the dysfunction of GABAergic inhibition in the motor circuits in the basal ganglia. |
