PARKINSONIAN-LIKE LOCOMOTOR IMPAIRMENT IN MICE LACKING DOPAMINE D2 RECEPTORS

DOPAMINERGIC neuronal pathways arise from mesencephalic nuclei and pro ject axons to the striatum, cortex, limbic system and hypothalamus(1,2 ). Through these pathways dopamine affects many physiological function s, such as the control of coordinated movement and hormone secretion(3 ). Here we have studied the physiological involvement of the dopamine D2 receptors in dopaminergic transmission, using homologous recombinat ion to generate D2-receptor-deficient mice. Absence of D2 receptors le ads to animals that are akinetic and bradykinetic in behavioural tests , and which show significantly reduced spontaneous movements. This phe notype presents analogies with symptoms characteristic of Parkinson's disease(4,5). Our study shows that D2 receptors have a key role in the dopaminergic control of nervous function. These mice have therapeutic potential as a model for investigating and correcting dysfunctions of the dopaminergic system.