Medial prefrontal D1 dopamine neurons control food intake

Nat Neurosci. 2014 Feb;17(2):248-53. doi: 10.1038/nn.3625. Epub 2014 Jan 19.

Abstract

Although the prefrontal cortex influences motivated behavior, its role in food intake remains unclear. Here, we demonstrate a role for D1-type dopamine receptor-expressing neurons in the medial prefrontal cortex (mPFC) in the regulation of feeding. Food intake increases activity in D1 neurons of the mPFC in mice, and optogenetic photostimulation of D1 neurons increases feeding. Conversely, inhibition of D1 neurons decreases intake. Stimulation-based mapping of prefrontal D1 neuron projections implicates the medial basolateral amygdala (mBLA) as a downstream target of these afferents. mBLA neurons activated by prefrontal D1 stimulation are CaMKII positive and closely juxtaposed to prefrontal D1 axon terminals. Finally, photostimulating these axons in the mBLA is sufficient to increase feeding, recapitulating the effects of mPFC D1 stimulation. These data describe a new circuit for top-down control of food intake.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Amygdala / metabolism
  • Analysis of Variance
  • Animals
  • Biophysics
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism
  • Channelrhodopsins
  • Eating / genetics
  • Eating / physiology*
  • Electric Stimulation
  • Female
  • Food Deprivation / physiology
  • Functional Laterality
  • Gene Expression Regulation / genetics
  • In Vitro Techniques
  • Luminescent Proteins / genetics
  • Male
  • Membrane Potentials / drug effects
  • Membrane Potentials / genetics
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neural Inhibition / genetics
  • Neural Inhibition / radiation effects
  • Neural Pathways / physiology
  • Neurons / metabolism*
  • Optogenetics
  • Patch-Clamp Techniques
  • Photic Stimulation / adverse effects
  • Prefrontal Cortex / cytology*
  • Receptors, Dopamine D1 / genetics
  • Receptors, Dopamine D1 / metabolism*
  • Time Factors

Substances

  • Channelrhodopsins
  • Drd1 protein, mouse
  • Luminescent Proteins
  • Receptors, Dopamine D1
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2