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  • Dopamine-Deficient Mice Are Severely Hypoactive, Adipsic, and Aphagic
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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.

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