Lack of Medial Prefrontal Cortex Activation Underlies the Immediate Extinction Deficit

• Published in: The Journal of neuroscience Vol. 30; no. 3; pp. 832 - 837
• Main Authors: Kim, Seok Chan, Jo, Yong Sang, Kim, Il Hwan, Kim, Hyun, Choi, June-Seek
• Format: Journal Article
• Language: English
• Published: United States Soc Neuroscience 20-01-2010; Society for Neuroscience
• Subjects: Acoustic Stimulation - adverse effects; Afferent Pathways - physiology; Analysis of Variance; Animals; Brief Communications; Cell Count - methods; Conditioning, Classical - physiology; Electroshock - adverse effects; Extinction, Psychological - physiology; Gene Expression Regulation - physiology; Indoles; Limbic System - physiology; Oncogene Proteins v-fos - metabolism; Prefrontal Cortex - metabolism; Rats; Reaction Time - physiology; Time Factors
• ISSN: 0270-6474; 1529-2401; 1529-2401
• DOI: 10.1523/JNEUROSCI.4145-09.2010

We conducted a series of experiments to investigate the neural basis of the immediate extinction deficit, the lack of extinction when the interval between fear memory acquisition and extinction is short. In experiment 1, rats were given extinction training composed of 15 conditioned stimuli (CSs) either 15 min (immediate extinction: I-EXT) or 24 h (delayed extinction: D-EXT) after five tone-shock pairings. In the retention test performed 48 h after conditioning, I-EXT group exhibited significantly higher freezing than D-EXT group. In experiment 2, functional activation in the medial prefrontal cortex (mPFC) was detected using c-fos immunoreactivity. The number of Fos-positive neurons in the mPFC was significantly lower in I-EXT group than in D-EXT group. In experiment 3, rats received immediate extinction with microstimulation of the infralimbic region (IL) of the mPFC, either contingently paired or unpaired with the CS. In a subsequent retention test, the paired stimulation group exhibited decreased freezing relative to the unpaired stimulation group. Together, our results suggest that the immediate extinction deficit may be linked to the lack of neuronal activity in the IL.