Child pages
  • Dopamine-Deficient Mice Are Severely Hypoactive, Adipsic, and Aphagic
Skip to end of metadata
Go to start of metadata


The authors of this article studied the effects of dopamine on feeding behavior by eliminating tyrosine hydroxylase, the enzyme that converts L-tyrosine to L-DOPA in the catecholamine synthesis pathway. They then gave L-DOPA supplements to mice that lacked tyrosine hydroxylase in the dopaminergic enzymes to rescue the deficits. This figure demonstrates the differences in food/water intake and body weight between control mice and DA-/- mice and then shows changes that occur upon L-DOPA administration. The L-DOPA administration effectively restores dopamine transmission, as it bypasses the tyrosine hydroxylase step in the synthesis pathway. Mice without dopamine are unable to initiate feeding (or drinking - adipsia) and their body weights rapidly decline. However, they become similar to control mice after L-DOPA restores the dopaminergic circuitry. This experiment provides convincing evidence that dopamine is a requirement for normal feeding habits; the dopaminergic circuitry might be implicated in feeding behavior gone awry. These results are similar to those seen in the Kim et al. paper in that D2R-/- mice eat less and weigh less than control mice. Clearly, the presence or absence of dopamine has implications for feeding behavior.

Return to Neural Reward, Energy Homeostasis, and Addiction-like Compulsive Eating

  • No labels