Basolateral amygdala lesions abolish orbitofrontal-dependent reversal impairments

Neuron. 2007 Apr 5;54(1):51-8. doi: 10.1016/j.neuron.2007.02.014.


Damage to orbitofrontal cortex (OFC) has long been associated with deficits in reversal learning. OFC damage also causes inflexible associative encoding in basolateral amygdala (ABL) during reversal learning. Here we provide a critical test of the hypothesis that the reversal deficit in OFC-lesioned rats is caused by this inflexible encoding in ABL. Rats with bilateral neurotoxic lesions of OFC, ABL, or both areas were tested on a series of two-odor go/no-go discrimination problems, followed by two serial reversals of the final problem. As expected, all groups acquired the initial problems at the same rate, and rats with OFC lesions were slower to acquire the reversals than sham controls. This impairment was abolished by accompanying ABL lesions, while ABL lesions alone had no effect on reversal learning. These results are consistent with the hypothesis that OFC facilitates cognitive flexibility by promoting updating of associative encoding in downstream brain areas.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Amygdala / injuries
  • Amygdala / physiopathology*
  • Analysis of Variance
  • Animals
  • Behavior, Animal
  • Brain Injuries / chemically induced
  • Brain Injuries / pathology*
  • Brain Injuries / physiopathology*
  • Choice Behavior / drug effects
  • Choice Behavior / physiology
  • Discrimination Learning / drug effects
  • Discrimination Learning / physiology
  • Frontal Lobe / injuries
  • Frontal Lobe / physiopathology*
  • Male
  • N-Methylaspartate / toxicity
  • Odorants
  • Rats
  • Rats, Long-Evans
  • Reversal Learning / drug effects
  • Reversal Learning / physiology*


  • N-Methylaspartate