Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors

DOPAMINERGIC neuronal pathways arise from mesencephalic nuclei and project axons to the striatum, cortex, limbic system and hypothalamus^1,2. Through these pathways dopamine affects many physiological functions, such as the control of coordinated movement and hormone secretion³. Here we have studied the physiological involvement of the dopamine D2 receptors in dopaminergic transmission, using homologous recombination to generate D2-receptor-deficient mice. Absence of D2 receptors leads to animals that are akinetic and bradykinetic in behavioural tests, and which show significantly reduced spontaneous movements. This pheno-type presents analogies with symptoms characteristic of Parkin-son'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.