Central amygdala PKC-δ(+) neurons mediate the influence of multiple anorexigenic signals

Nat Neurosci. 2014 Sep;17(9):1240-8. doi: 10.1038/nn.3767. Epub 2014 Jul 27.


Feeding can be inhibited by multiple cues, including those associated with satiety, sickness or unpalatable food. How such anorexigenic signals inhibit feeding at the neural circuit level is not completely understood. Although some inhibitory circuits have been identified, it is not yet clear whether distinct anorexigenic influences are processed in a convergent or parallel manner. The amygdala central nucleus (CEA) has been implicated in feeding control, but its role is controversial. The lateral subdivision of CEA (CEl) contains a subpopulation of GABAergic neurons that are marked by protein kinase C-δ (PKC-δ). We found that CEl PKC-δ(+) neurons in mice were activated by diverse anorexigenic signals in vivo, were required for the inhibition of feeding by such signals and strongly suppressed food intake when activated. They received presynaptic inputs from anatomically distributed neurons activated by different anorexigenic agents. Our data suggest that CEl PKC-δ(+) neurons constitute an important node that mediates the influence of multiple anorexigenic signals.

Publication types

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

MeSH terms

  • Action Potentials / physiology
  • Animals
  • Anorexia / metabolism*
  • Anxiety / metabolism
  • Central Amygdaloid Nucleus / physiology*
  • Feeding Behavior / physiology
  • GABAergic Neurons / physiology*
  • Male
  • Maze Learning / physiology
  • Mice
  • Neural Inhibition / physiology
  • Optogenetics
  • Presynaptic Terminals / metabolism
  • Protein Kinase C-delta / metabolism*
  • Satiety Response / physiology
  • Signal Transduction / physiology*


  • Protein Kinase C-delta