PT  - JOURNAL ARTICLE
AU  - Anthony Burgos-Robles
AU  - Ivan Vidal-Gonzalez
AU  - Gregory J. Quirk
TI  - Sustained Conditioned Responses in Prelimbic Prefrontal Neurons Are Correlated with Fear Expression and Extinction Failure
AID  - 10.1523/JNEUROSCI.0378-09.2009
DP  - 2009 Jul 01
TA  - The Journal of Neuroscience
PG  - 8474--8482
VI  - 29
IP  - 26
4099  - http://www.jneurosci.org/content/29/26/8474.short
4100  - http://www.jneurosci.org/content/29/26/8474.full
SO  - J. Neurosci.2009 Jul 01; 29
AB  - During auditory fear conditioning, it is well established that lateral amygdala (LA) neurons potentiate their response to the tone conditioned stimulus, and that this potentiation is required for conditioned fear behavior. Conditioned tone responses in LA, however, last only a few hundred milliseconds and cannot be responsible for sustained fear responses to a tone lasting tens of seconds. Recent evidence from inactivation and stimulation studies suggests that the prelimbic (PL) prefrontal cortex is necessary for expression of learned fears, but the timing of PL tone responses and correlations with fear behavior have not been studied. Using multichannel unit recording techniques in behaving rats, we observed sustained conditioned tone responses in PL that were correlated with freezing behavior on a second-to-second basis during the presentation of a 30 s tone. PL tone responses were also correlated with conditioned freezing across different experimental phases (habituation, conditioning, extinction). Moreover, the persistence of PL responses after extinction training was associated with failure to express extinction memory. Together with previous inactivation findings, the present results suggest that PL transforms transient amygdala inputs to a sustained output that drives conditioned fear responses and gates the expression of extinction. Given the relatively long latency of conditioned responses we observed in PL (∼100 ms after tone onset), we propose that PL integrates inputs from the amygdala, hippocampus, and other cortical sources to regulate the expression of fear memories.