The role of the basolateral amygdala and infralimbic cortex in (re)learning extinction

• Published in: Psychopharmacology Vol. 236; no. 1; pp. 303 - 312
• Main Authors: Lingawi, Nura W., Laurent, Vincent, Westbrook, R. Fredrick, Holmes, Nathan M.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 2019; Springer; Springer Nature B.V
• Subjects: Amygdala; Amygdala (Brain); Biomedical and Life Sciences; Biomedicine; Brain; Conditioned stimulus; Conditioning; Cortex (temporal); Endangered species; Exposure; Extinction (Psychology); Extinction behavior; Fear conditioning; Laboratories; Learning; Memory; Neurological research; Neurons; Neurosciences; Novels; Pharmacology/Toxicology; Physiological aspects; Prefrontal cortex; Psychiatry; Reconditioning; Review; Rodents; Stimulation; Learning; Basolateral amygdala complex; Relearning; Conditioned fear; Extinction; Infralimbic cortex
• ISSN: 0033-3158; 1432-2072
• DOI: 10.1007/s00213-018-4957-x

The basolateral amygdala complex (BLA) and infralimbic region of the prefrontal cortex (IL) play distinct roles in the extinction of Pavlovian conditioned fear in laboratory rodents. In the past decade, research in our laboratory has examined the roles of these brain regions in the re- extinction of conditioned fear: i.e., extinction of fear that is restored through re-conditioning of the conditioned stimulus (CS) or changes in the physical and temporal context of extinction training (i.e., extinction of renewed or spontaneously recovered fear). This paper reviews this research. It has revealed two major findings. First, in contrast to the acquisition of fear extinction, which usually requires neuronal activity in the BLA but not IL, the acquisition of fear re-extinction requires neuronal activity in the IL but can occur independently of neuronal activity in the BLA. Second, the role of the IL in fear extinction is determined by the training history of the CS: i.e., if the CS was novel prior to its fear conditioning (i.e., it had not been trained), the acquisition of fear extinction does not require the IL; if, however, the prior training of the CS included a series of CS-alone exposures (e.g., if the CS had been pre-exposed), the acquisition of fear extinction was facilitated by pharmacological stimulation of the IL. Together, these results were taken to imply that a memory of CS-alone exposures is stored in the IL, survives fear conditioning of the CS, and can be retrieved and strengthened during extinction or re-extinction of that CS (regardless of whether the extinction is first- or second-learned). Hence, under these circumstances, the initial extinction of fear to the CS can be facilitated by pharmacological stimulation of the IL, and re-extinction of fear to the CS can occur in the absence of a functioning BLA.