Literature search services are currently unavailable. During our hosting provider's UPS upgrade we experienced a hardware failure and are currently working to resolve the issue.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Dopamine-deficient mice are severely hypoactive, adipsic, and aphagic.

Mice unable to synthesize dopamine (DA) specifically in dopaminergic neurons were created by inactivating the tyrosine hydroxylase (TH) gene then by restoring TH function in noradrenergic cells. These DA-deficient (DA-/-) mice were born at expected frequency but became hypoactive and stopped feeding a few weeks after birth. Midbrain dopaminergic neurons, their projections, and most characteristics of their target neurons in the striatum appeared normal. Within a few minutes of being injected with L-dihdroxyphenylalanine (L-DOPA), the product of TH, the DA-/- mice became more active and consumed more food than control mice. With continued administration of L-DOPA, nearly normal growth was achieved. These studies indicate that DA is essential for movement and feeding, but is not required for the development of neural circuits that control these behaviors.

Pubmed ID: 8548806


  • Zhou QY
  • Palmiter RD



Publication Data

December 29, 1995

Associated Grants

  • Agency: NICHD NIH HHS, Id: HD-09172

Mesh Terms

  • Adrenergic Fibers
  • Animals
  • Animals, Newborn
  • Behavior, Animal
  • Dopamine
  • Dopamine beta-Hydroxylase
  • Drinking Behavior
  • Dynorphins
  • Embryo, Mammalian
  • Feeding Behavior
  • Immunohistochemistry
  • In Situ Hybridization
  • Levodopa
  • Mesencephalon
  • Mice
  • Mice, Transgenic
  • Mutation
  • Neostriatum
  • Neurons
  • Norepinephrine
  • Substance P
  • Transgenes
  • Tyrosine 3-Monooxygenase