Stalnaker Thomas A, Franz Theresa M, Singh Teghpal, Schoenbaum Geoffrey
Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
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.
眶额皮质（OFC）受损长期以来一直与逆向学习缺陷有关。OFC损伤还会在逆向学习过程中导致基底外侧杏仁核（ABL）出现僵化的联想编码。在此，我们对以下假设进行了关键测试：OFC损伤大鼠的逆向学习缺陷是由ABL中的这种僵化编码所致。对患有双侧OFC、ABL或两个区域神经毒性损伤的大鼠进行了一系列双气味“走/停”辨别问题测试，随后对最终问题进行了两次连续反转。正如预期的那样，所有组以相同的速度掌握了初始问题，与假手术对照组相比，OFC损伤的大鼠掌握反转的速度较慢。伴随的ABL损伤消除了这种损伤，而单独的ABL损伤对逆向学习没有影响。这些结果与以下假设一致：OFC通过促进下游脑区联想编码的更新来促进认知灵活性。
